First_Aid_Step1

First_Aid_Step1. Lateral lesions—affect voluntary movement of extremities (lateral structures); when injured, propensity to fall toward injured (ipsilateral) side. Medial lesions (eg, vermis, fastigial nuclei, flocculonodular lobe)—truncal ataxia (widebased cerebellar gait), nystagmus, head tilting. Generally result in bilateral motor deficits affecting axial and proximal limb musculature (medial structures). Important in voluntary movements and adjusting posture A . D1 Receptor = D1Rect Receives cortical input, provides negative feedback to cortex to pathway. modulate movement. Indirect (D2) = Inhibitory. Striatum = putamen (motor) + Caudate (cognitive). Lentiform = putamen + globus pallidus. Direct (excitatory) pathway—SNc input to the striatum via the nigrostriatal dopaminergic pathway releases GABA, which inhibits GABA release from the GPi, disinhibiting the Thalamus via the GPi (• motion).


First_Aid_Step1

First_Aid_Step1. Indirect (inhibitory) pathway—SNc input to the striatum via the nigrostriatal dopaminergic pathway releases GABA that disinhibits STN via GPe inhibition, and STN stimulates GPi to inhibit the thalamus (• motion). Dopamine binds to D1, stimulating the excitatory pathway, and to D2, inhibiting the inhibitory pathway  motion. Cerebral perfusion Relies on tight autoregulation. Primarily driven by Pco2 (Po2 also modulates perfusion in severe hypoxia). Also relies on a pressure gradient between mean arterial pressure (MAP) and intracranial pressure (ICP).  blood pressure or  ICP  cerebral perfusion pressure (CPP).  vasoconstriction  cerebral blood flow  ICP. May be used to treat acute cerebral edema (eg, 2° to stroke) unresponsive to other interventions. CPP = MAP – ICP. If CPP = 0, there is no cerebral perfusion • brain death. Hypoxemia increases CPP only if Po2 < 50 mm Hg. CPP is directly proportional to Pco2 until Pco2 > 90 mm Hg.


First_Aid_Step1

First_Aid_Step1. CPP = MAP – ICP. If CPP = 0, there is no cerebral perfusion • brain death. Hypoxemia increases CPP only if Po2 < 50 mm Hg. CPP is directly proportional to Pco2 until Pco2 > 90 mm Hg. HipLeg HipTrunk NeckHeadShoulderArmElbow RingLittle MiddleIndexThumb ForearmWrist Toes Ankle KneeShoulder FingersFingers ElbowWristHandLittleRingMiddleIndexThumbNeckBrow Lips TongueJaw Swallowing Eyelid & eyeball TrunkEye Nose Face Upper lip Lower lipTeeth, gums Foot Toes TongueIntra-abdominalPharynx Genitals Homunculus Topographic representation of motor and sensory areas in the cerebral cortex. Distorted appearance is due to certain body regions being more richly innervated and thus having  cortical representation. Watershed zones Cortical border zones occur between anterior and middle cerebral arteries and posterior and middle cerebral arteries (blue areas in A ). Internal border zones occur between the superficial and deep vascular territories of the middle cerebral artery (red areas in A ).


First_Aid_Step1

First_Aid_Step1. A ). Infarct due to severe hypoperfusion • proximal upper and lower extremity weakness (“manin-the-barrel syndrome”), higher order visual dysfunction (if posterior cerebral/middle cerebral cortical border zone stroke). Circle of Willis System of anastomoses between anterior and posterior blood supplies to brain. Dural venous sinuses Large venous channels A that run through the periosteal and meningeal layers of the dura mater. Drain blood from cerebral veins (arrow) and receive CSF from arachnoid granulations. Empty into internal jugular vein. Venous sinus thrombosis—presents with signs/symptoms of • ICP (eg, headache, seizures, papilledema, focal neurologic deficits). May lead to venous hemorrhage. Associated with hypercoagulable states (eg, pregnancy, OCP use, factor V Leiden). (main location of CSF return via arachnoid granulations) Superior ophthalmic vein Great cerebral vein of Galen Confuence of the sinuses Sigmoid sinus


First_Aid_Step1

First_Aid_Step1. (main location of CSF return via arachnoid granulations) Superior ophthalmic vein Great cerebral vein of Galen Confuence of the sinuses Sigmoid sinus Lateral ventricles  3rd ventricle via right and left interventricular foramina of Monro. 3rd ventricle  4th ventricle via cerebral aqueduct of Sylvius. 4th ventricle  subarachnoid space via: Foramina of Luschka = Lateral. Foramen of Magendie = Medial. CSF made by choroid plexuses located in the lateral and fourth ventricles. Travels to subarachnoid space via foramina of Luschka and Magendie, is reabsorbed by arachnoid granulations, and then drains into dural venous sinuses. Brain stem—ventral view 4 CN are above pons (I, II, III, IV). 4 CN exit the pons (V, VI, VII, VIII). (CN I) 4 CN are in medulla (IX, X, XI, XII). Olfactory tract 4 CN nuclei are medial (III, IV, VI, XII). CN II “Factors of 12, except 1 and 2.” Middle cerebellar Anterior wall of peduncle fourth ventricle


First_Aid_Step1

First_Aid_Step1. Middle cerebellar Anterior wall of peduncle fourth ventricle Pineal gland—melatonin secretion, circadian rhythms. Superior colliculi—direct eye movements to stimuli (noise/movements) or objects of interest. Inferior colliculi—auditory. Your eyes are above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory). In adults, spinal cord ends at lower border of L1–L2 vertebrae. Subarachnoid Space (which contains the CSF) extends to lower border of S2 vertebra. Lumbar puncture is usually performed between L3–L4 or L4–L5 (level of cauda equina). Goal of lumbar puncture is to obtain sample of CSF without damaging spinal cord. To keep the cord alive, keep the spinal needle between L3 and L5. Needle passes through: skin fascia and fat supraspinous ligament interspinous ligament ligamentum flavum epidural space (epidural anesthesia needle stops here) dura mater arachnoid mater subarachnoid space (CSF collection occurs here)


First_Aid_Step1

First_Aid_Step1. Spinal tract anatomy Ascending tracts synapse and then cross. and functions Dorsal column Pressure, vibration, fine touch, proprioception Spinothalamic tract Lateral: pain, temperature Anterior: crude touch, pressure Sensory nerve ending  bypasses pseudounipolar cell body in dorsal root ganglion  enters spinal cord  ascends ipsilaterally in dorsal columns Sensory nerve ending (Aδ and C fibers)  bypasses pseudounipolar cell body in dorsal root ganglion • enters spinal cord Nucleus gracilis, nucleus cuneatus (ipsilateral medulla)  ascends contralaterally as the medial lemniscus Decussates in spinal cord as the anterior white commissure Clinical reflexes Reflexes count up in order (main nerve root in Additional reflexes: bold): Cremasteric reflex = L1, L2 (“testicles move”) Achilles reflex = S1, S2 (“buckle my shoe”) Anal wink reflex = S3, S4 (“winks galore”) C5, 6


First_Aid_Step1

First_Aid_Step1. Patellar reflex = L2-L4 (“kick the door”) C6, 7, 8 Biceps and brachioradialis reflexes = C5, C6 (“pick up sticks”) L2, 3, 4 Triceps reflex = C6, C7, C8 (“lay them S1, 2 straight”) Primitive reflexes CNS reflexes that are present in a healthy infant, but are absent in a neurologically intact adult. Normally disappear within 1st year of life. These primitive reflexes are inhibited by a mature/ developing frontal lobe. They may reemerge in adults following frontal lobe lesions  loss of inhibition of these reflexes. Moro reflex “Hang on for life” reflex—abduct/extend arms when startled, and then draw together Rooting reflex Movement of head toward one side if cheek or mouth is stroked (nipple seeking) Sucking reflex Sucking response when roof of mouth is touched Palmar reflex Curling of fingers if palm is stroked


First_Aid_Step1

First_Aid_Step1. Sucking reflex Sucking response when roof of mouth is touched Palmar reflex Curling of fingers if palm is stroked Plantar reflex Dorsiflexion of large toe and fanning of other toes with plantar stimulation Babinski sign—presence of this reflex in an adult, which may signify a UMN lesion Galant reflex Stroking along one side of the spine while newborn is in ventral suspension (face down) causes lateral flexion of lower body toward stimulated side C2 Posterior half of skull C3 High turtleneck shirt Diaphragm and gallbladder pain referred to the right shoulder via phrenic nerve C3, 4, 5 keeps the diaphragm alive T4 At the nipple T4 at the teat pore T7 At the xiphoid process 7 letters in xiphoid T10 At the umbilicus (belly butten) Point of referred pain in early appendicitis L1 At the Inguinal Ligament L4 Includes the kneecaps Down on ALL 4’s S2, S3, S4 Sensation of penile and anal zones S2, 3, 4 keep the penis off the floor


First_Aid_Step1

First_Aid_Step1. L1 At the Inguinal Ligament L4 Includes the kneecaps Down on ALL 4’s S2, S3, S4 Sensation of penile and anal zones S2, 3, 4 keep the penis off the floor Irreversible neuronal injury begins after 5 minutes of hypoxia. Most vulnerable: hippocampus, neocortex, cerebellum (Purkinje cells), watershed areas (“vulnerable hippos need pure water”). Stroke imaging: noncontrast CT to exclude hemorrhage (before tPA can be given). CT detects ischemic changes in 6–24 hr. Diffusion-weighted MRI can detect ischemia within 3–30 min. Acute blockage of vessels  disruption of blood flow and subsequent ischemia  infarction necrosis. 3 types: Thrombotic—due to a clot forming directly at site of infarction (commonly the MCA A ), usually over a ruptured atherosclerotic plaque. Embolic—embolus from another part of the body obstructs vessel. Can affect multiple vascular territories. Examples: atrial fibrillation, carotid artery stenosis, DVT with patent foramen ovale, infective endocarditis.


First_Aid_Step1

First_Aid_Step1. Hypoxic—due to hypoperfusion or hypoxemia. Common during cardiovascular surgeries, tends to affect watershed areas. Treatment: tPA (if within 3–4.5 hr of onset and no hemorrhage/risk of hemorrhage) and/or thrombectomy (if large artery occlusion). Reduce risk with medical therapy (eg, aspirin, clopidogrel); optimum control of blood pressure, blood sugars, lipids; smoking cessation; and treat conditions that  risk (eg, atrial fibrillation, carotid artery stenosis). Transient ischemic Brief, reversible episode of focal neurologic dysfunction without acute infarction (⊝ MRI), with the attack majority resolving in < 15 minutes; ischemia (eg, embolus, small vessel stenosis).


First_Aid_Step1

First_Aid_Step1. Bleeding into ventricles (arrow in coronal transcranial ultrasound A shows blood in right intraventricular space, extending into periventricular white matter). Increased risk in premature and low-birth-weight infants. Originates in germinal matrix, a highly vascularized layer within the subventricular zone. Due to reduced glial fiber support and impaired autoregulation of BP in premature infants. Can present with altered level of consciousness, bulging fontanelle, hypotension, seizures, coma. Epidural hematoma Rupture of middle meningeal artery (branch of maxillary artery), often 2° to skull fracture (circle in A ) involving the pterion (thinnest area of the lateral skull). Might present with transient loss of consciousness  recovery (“lucid interval”)  rapid deterioration due to hematoma expansion. Scalp hematoma (arrows in


First_Aid_Step1

First_Aid_Step1. A ) and rapid intracranial expansion (arrows in B ) under systemic arterial pressure  transtentorial herniation, CN III palsy. CT shows biconvex (lentiform), hyperdense blood collection B not crossing suture lines. Subdural hematoma Rupture of bridging veins. Can be acute (traumatic, high-energy impact  hyperdense on CT) or chronic (associated with mild trauma, cerebral atrophy, elderly, alcoholism  hypodense on CT). Also seen in shaken babies. Predisposing factors: brain atrophy, trauma. Crescent-shaped hemorrhage (red arrows in C and D ) that crosses suture lines. Can cause midline shift (yellow arrow in C ), findings of “acute on chronic” hemorrhage (blue arrows in D ).


First_Aid_Step1

First_Aid_Step1. Crescent-shaped hemorrhage (red arrows in C and D ) that crosses suture lines. Can cause midline shift (yellow arrow in C ), findings of “acute on chronic” hemorrhage (blue arrows in D ). EF due to trauma, or rupture of an aneurysm (such as a saccular aneurysm E ) or arteriovenous malformation. Rapid time course. Patients complain of “worst headache of my life.” Bloody or yellow (xanthochromic) lumbar puncture. Vasospasm can occur due to blood breakdown  ischemic infarct; nimodipine used to prevent/reduce vasospasm.  risk of developing communicating and/or obstructive hydrocephalus. Most commonly caused by systemic hypertension. Also seen with amyloid angiopathy (recurrent lobar hemorrhagic stroke in elderly), vasculitis, neoplasm. May be 2º to reperfusion injury in ischemic stroke. Hypertensive hemorrhages (Charcot-Bouchard microaneurysm) most often occur in putamen of basal ganglia (lenticulostriate vessels G ), followed by thalamus, pons, and cerebellum H .


First_Aid_Step1

First_Aid_Step1. Hypertensive hemorrhages (Charcot-Bouchard microaneurysm) most often occur in putamen of basal ganglia (lenticulostriate vessels G ), followed by thalamus, pons, and cerebellum H . Effects of strokes Anterior circulation Middle cerebral artery Motor and sensory cortices A —upper limb and face. Temporal lobe (Wernicke area); frontal lobe (Broca area). Contralateral paralysis and sensory loss—face and upper limb. Aphasia if in dominant (usually left) hemisphere. Hemineglect if lesion affects nondominant (usually right) hemisphere. Wernicke aphasia is associated with right superior quadrant visual field defect due to temporal lobe involvement. Lenticulo-striate artery Striatum, internal capsule. Contralateral paralysis. Absence of cortical signs (eg, neglect, aphasia, visual field loss). Pure motor stroke. Common location of lacunar infarcts B , due to hyaline arteriosclerosis (lipohyalinosis) 2° to unmanaged hypertension. Posterior circulation


First_Aid_Step1

First_Aid_Step1. Lateral medulla: Nucleus ambiguus (CN IX, X, XI) Vestibular nuclei Lateral spinothalamic tract, spinal trigeminal nucleus Dysphagia, hoarseness, • gag reflex, hiccups. Vomiting, vertigo, nystagmus  pain and temperature sensation from contralateral body, ipsilateral face. Ipsilateral Horner syndrome. Ipsilateral ataxia, dysmetria. Lateral medullary (Wallenberg) syndrome. Nucleus ambiguus effects are specific to PICA lesions C . “Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia).” Also supplies inferior cerebellar peduncle (part of cerebellum). Lateral pons: Facial nucleus Vestibular nuclei Spinothalamic tract, spinal trigeminal nucleus Paralysis of face (LMN lesion vs UMN lesion in cortical stroke),  lacrimation,  salivation, • taste from anterior 2⁄3 of tongue. Vomiting, vertigo, nystagmus  pain and temperature sensation from contralateral body, ipsilateral face. Ipsilateral Horner syndrome. Ipsilateral ataxia, dysmetria.


First_Aid_Step1

First_Aid_Step1. Ipsilateral Horner syndrome. Ipsilateral ataxia, dysmetria. Ipsilateral sensorineural deafness, vertigo. Lateral pontine syndrome. Facial nucleus effects are specific to AICA lesions. “Facial droop means AICA’s pooped.” Also supplies middle and inferior cerebellar peduncles (part of cerebellum). Effects of strokes (continued) Basilar artery Pons, medulla, lower midbrain. Corticospinal and corticobulbar tracts. Ocular cranial nerve nuclei, paramedian pontine reticular formation. If RAS spared, consciousness is preserved. Quadriplegia; loss of voluntary facial, mouth, and tongue movements. Loss of horizontal, but not vertical, eye movements. Locked-in syndrome (locked in the basement). Posterior cerebral artery Occipital lobe D . Contralateral hemianopia with macular sparing; alexia without agraphia (dominant hemisphere).


First_Aid_Step1

First_Aid_Step1. Locked-in syndrome (locked in the basement). Posterior cerebral artery Occipital lobe D . Contralateral hemianopia with macular sparing; alexia without agraphia (dominant hemisphere). Diffuse axonal injury Caused by traumatic shearing forces during rapid acceleration and/or deceleration of the brain (eg, motor vehicle accident). Usually results in devastating neurologic injury, often causing coma or persistent vegetative state. MRI A shows multiple lesions (punctate hemorrhages) involving the white matter tracts. Aphasia Aphasia—higher-order language deficit Good comprehension Poor comprehension (inability to understand/produce/use language appropriately); caused by pathology in dominant cerebral hemisphere (usually left). speech Dysarthria—motor inability to produce speech (movement deficit). Broca (expressive) Broca area in inferior frontal gyrus of frontal lobe. Patient appears frustrated, insight intact. Broca = Broken Boca (boca = mouth in Spanish).


First_Aid_Step1

First_Aid_Step1. Broca (expressive) Broca area in inferior frontal gyrus of frontal lobe. Patient appears frustrated, insight intact. Broca = Broken Boca (boca = mouth in Spanish). Wernicke (receptive) Wernicke area in superior temporal gyrus of temporal lobe. Patients do not have insight. Wernicke is a Word salad and makes no sense. Conduction Can be caused by damage to arCuate fasciculus. Global Broca and Wernicke areas affected. Transcortical motor Affects frontal lobe around Broca area, but Broca area is spared. Transcortical sensory Affects temporal lobe around Wernicke area, but Wernicke area is spared. Transcortical mixed Broca and Wernicke areas and arcuate fasciculus remain intact; surrounding watershed areas affected. Aneurysms Abnormal dilation of an artery due to weakening of vessel wall.


First_Aid_Step1

First_Aid_Step1. Transcortical mixed Broca and Wernicke areas and arcuate fasciculus remain intact; surrounding watershed areas affected. Aneurysms Abnormal dilation of an artery due to weakening of vessel wall. Also called berry aneurysm A . Occurs at bifurcations in the circle of Willis. Most common site is junction of ACom and ACA. Associated with ADPKD, Ehlers-Danlos syndrome. Other risk factors: advanced age, hypertension, smoking, race ( risk in African-Americans). Usually clinically silent until rupture (most common complication) • subarachnoid hemorrhage (“worst headache of my life” or “thunderclap headache”)  focal neurologic deficits. Can also cause symptoms via direct compression of surrounding structures by growing aneurysm. ACom—compression  bitemporal hemianopia (compression of optic chiasm); visual acuity deficits; rupture  ischemia in ACA distribution • contralateral lower extremity hemiparesis, sensory deficits.


First_Aid_Step1

First_Aid_Step1. ACom—compression  bitemporal hemianopia (compression of optic chiasm); visual acuity deficits; rupture  ischemia in ACA distribution • contralateral lower extremity hemiparesis, sensory deficits. MCA—rupture  ischemia in MCA distribution  contralateral upper extremity and lower facial hemiparesis, sensory deficits. PCom—compression  ipsilateral CN III palsy • mydriasis (“blown pupil”); may also see ptosis, “down and out” eye. Seizures Characterized by synchronized, high-frequency neuronal firing. Variety of forms. Impaired consciousness? Headaches Pain due to irritation of structures such as the dura, cranial nerves, or extracranial structures. More common in females, except cluster headaches. Unilateral 15 min–3 hr; Excruciating periorbital pain repetitive (“suicide headache”) with lacrimation and rhinorrhea. May present with Horner syndrome. More common in males.


First_Aid_Step1

First_Aid_Step1. Unilateral 15 min–3 hr; Excruciating periorbital pain repetitive (“suicide headache”) with lacrimation and rhinorrhea. May present with Horner syndrome. More common in males. Unilateral 4–72 hr Pulsating pain with nausea, photophobia, or phonophobia. May have “aura.” Due to irritation of CN V, meninges, or blood vessels (release of vasoactive neuropeptides [eg, substance P, calcitonin gene-related peptide]). Bilateral > 30 min Steady, “band-like” pain. No (typically 4–6 photophobia or phonophobia. hr); constant No aura. Acute: sumatriptan, 100% O2. Prophylaxis: verapamil. Acute: NSAIDs, triptans, dihydroergotamine. Prophylaxis: lifestyle changes (eg, sleep, exercise, diet), β-blockers, amitriptyline, topiramate, valproate, botulinum toxin, anti-CGRP monoclonal antibodies. POUND–Pulsatile, One-day duration, Unilateral, Nausea, Disabling. Acute: analgesics, NSAIDs, acetaminophen. Prophylaxis: TCAs (eg, amitriptyline), behavioral therapy.


First_Aid_Step1

First_Aid_Step1. POUND–Pulsatile, One-day duration, Unilateral, Nausea, Disabling. Acute: analgesics, NSAIDs, acetaminophen. Prophylaxis: TCAs (eg, amitriptyline), behavioral therapy. Other causes of headache include subarachnoid hemorrhage (“worst headache of my life”), meningitis, hydrocephalus, neoplasia, giant cell (temporal) arteritis. aCompare with trigeminal neuralgia, which produces repetitive, unilateral, shooting/shock-like pain in the distribution of CN V. Triggered by chewing, talking, touching certain parts of the face. Lasts (typically) for seconds to minutes, but episodes often increase in intensity and frequency over time. First-line therapy: carbamazepine. Athetosis Slow, snake-like, writhing Basal ganglia. Seen in Huntington disease. movements; especially seen in the fingers. Intention tremor Slow, zigzag motion when Cerebellar dysfunction. pointing/extending toward a target.


First_Aid_Step1

First_Aid_Step1. Intention tremor Slow, zigzag motion when Cerebellar dysfunction. pointing/extending toward a target. Hemiballismus Sudden, wild flailing of one Contralateral subthalamic Pronounce “Half-of-body side of the body. nucleus (eg, lacunar stroke). ballistic.” Parkinson TRAPSS your body: Tremor (pill-rolling tremor at rest) Rigidity (cogwheel) Akinesia (or bradykinesia) Postural instability Shuffling gait Small handwriting (micrographia) MPTP, a contaminant in illegal drugs, is metabolized to MPP+, which is toxic to substantia nigra.  in cognitive ability, memory, or function with intact consciousness. Must rule out depression as cause of dementia (called pseudodementia). Other reversible causes of dementia: hypothyroidism, vitamin B12 deficiency, neurosyphilis, normal pressure hydrocephalus. Loss of dopaminergic neurons (ie, depigmentation) of substantia nigra pars compacta. Lewy bodies: composed of α-synuclein (intracellular eosinophilic inclusions A ).


First_Aid_Step1

First_Aid_Step1. Loss of dopaminergic neurons (ie, depigmentation) of substantia nigra pars compacta. Lewy bodies: composed of α-synuclein (intracellular eosinophilic inclusions A ). Autosomal dominant trinucleotide (CAG)n repeat expansion in the huntingtin (HTT) gene on chromosome 4 (4 letters). Symptoms manifest between ages 20 and 50: chorea, athetosis, aggression, depression, dementia (sometimes initially mistaken for substance abuse). Anticipation results from expansion of CAG repeats. Caudate loses ACh and GABA. Atrophy of caudate and putamen with ex vacuo ventriculomegaly. • dopamine,  GABA,  ACh in brain. Neuronal death via NMDA-R binding and glutamate excitotoxicity. Most common cause of dementia in elderly. Down syndrome patients have  risk of developing Alzheimer disease, as APP is located on chromosome 21. ACh. Associated with the following altered proteins: ApoE-2:  risk of sporadic form


First_Aid_Step1

First_Aid_Step1. ACh. Associated with the following altered proteins: ApoE-2:  risk of sporadic form ApoE-4:  risk of sporadic form • APP, presenilin-1, presenilin-2: familial forms (10%) with earlier onset Widespread cortical atrophy (normal cortex B ; cortex in Alzheimer disease C ), especially hippocampus (arrows in B and C ). Narrowing of gyri and widening of sulci. Senile plaques D in gray matter: extracellular β-amyloid core; may cause amyloid angiopathy  intracranial hemorrhage; Aβ (amyloid-β) synthesized by cleaving amyloid precursor protein (APP). E : intracellular, hyperphosphorylated tau protein = insoluble cytoskeletal elements; number of tangles correlates with degree of dementia. Hirano bodies—intracellular eosinophilic proteinaceous rods in hippocampus. Formerly called Pick disease. Early changes in Frontotemporal lobe degeneration


First_Aid_Step1

First_Aid_Step1. Hirano bodies—intracellular eosinophilic proteinaceous rods in hippocampus. Formerly called Pick disease. Early changes in Frontotemporal lobe degeneration F . personality and behavior (behavioral variant), Inclusions of hyperphosphorylated tau (round or aphasia (primary progressive aphasia). Pick bodies G ) or ubiquitinated TDP-43. May have associated movement disorders. Lewy body dementia Visual hallucinations (“haLewycinations”), Intracellular Lewy bodies A primarily in cortex. dementia with fluctuating cognition/ alertness, REM sleep behavior disorder, and parkinsonism. Called Lewy body dementia if apart, otherwise considered dementia 2° to Parkinson disease.


First_Aid_Step1

First_Aid_Step1. dementia with fluctuating cognition/ alertness, REM sleep behavior disorder, and parkinsonism. Called Lewy body dementia if apart, otherwise considered dementia 2° to Parkinson disease. Also called pseudotumor cerebri.  ICP with no obvious findings on imaging. Risk factors include female sex, Tetracyclines, Obesity, vitamin A excess, Danazol (female TOAD). Associated with cerebral venous sinus stenosis. Findings: headache, tinnitus, diplopia (usually from CN VI palsy), no change in mental status. Impaired optic nerve axoplasmic flow  papilledema. Visual field testing shows enlarged blind spot and peripheral constriction. Lumbar puncture reveals • opening pressure and provides temporary headache relief. Treatment: weight loss, acetazolamide, invasive procedures for refractory cases (eg, CSF shunt placement, optic nerve sheath fenestration surgery for visual loss). Hydrocephalus  CSF volume  ventricular dilation +/− • ICP.


First_Aid_Step1

First_Aid_Step1. Hydrocephalus  CSF volume  ventricular dilation +/− • ICP. Noncommunicating Caused by structural blockage of CSF circulation within ventricular system (eg, stenosis of hydrocephalus aqueduct of Sylvius, colloid cyst blocking foramen of Monro, tumor B ). Multiple sclerosis Autoimmune inflammation and demyelination of CNS (brain and spinal cord) with subsequent axonal damage. Can present with: Acute optic neuritis (painful unilateral visual loss associated with Marcus Gunn pupil) Brain stem/cerebellar syndromes (eg, diplopia, ataxia, scanning speech, intention tremor, nystagmus/INO [bilateral > unilateral]) Pyramidal tract demyelination (eg, weakness, spasticity) Spinal cord syndromes (eg, electric shock-like sensation along cervical spine on neck flexion, neurogenic bladder, paraparesis, sensory manifestations affecting the trunk or one or more extremity)


First_Aid_Step1

First_Aid_Step1. Spinal cord syndromes (eg, electric shock-like sensation along cervical spine on neck flexion, neurogenic bladder, paraparesis, sensory manifestations affecting the trunk or one or more extremity) Symptoms may exacerbate with increased body temperature (eg, hot bath, exercise). Relapsing and remitting is most common clinical course. Most often affects women in their 20s and 30s; more common in individuals living farther from equator and with low serum vitamin D levels. Findings  IgG level and myelin basic protein in CSF. Oligoclonal bands are diagnostic. MRI is gold standard. Periventricular plaques A (areas of oligodendrocyte loss and reactive gliosis). Multiple white matter lesions disseminated in space and time.


First_Aid_Step1

First_Aid_Step1. treAtment Stop relapses and halt/slow progression with disease-modifying therapies (eg, β-interferon, glatiramer, natalizumab). Treat acute flares with IV steroids. Symptomatic treatment for neurogenic bladder (catheterization, muscarinic antagonists), spasticity (baclofen, GABAB receptor agonists), pain (TCAs, anticonvulsants). Osmotic demyelination Also called central pontine myelinolysis. Massive axonal demyelination in pontine white matter syndrome A 2° to rapid osmotic changes, most commonly iatrogenic correction of hyponatremia but also rapid shifts of other osmolytes (eg, glucose). Acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness. Can cause “locked-in syndrome.” Correcting serum Na+ too fast: “From low to high, your pons will die” (osmotic demyelination syndrome) “From high to low, your brains will blow” (cerebral edema/herniation)


First_Aid_Step1

First_Aid_Step1. Charcot-Marie-Tooth Also called hereditary motor and sensory neuropathy. Group of progressive hereditary nerve disease disorders related to the defective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath. Typically autosomal dominant and associated with foot deformities (eg, pes cavus, hammer toe), lower extremity weakness (eg, foot drop), and sensory deficits. Most common type, CMT1A, is caused by PMP22 gene duplication. Progressive multifocal Demyelination of CNS B due to destruction of oligodendrocytes (2° to reactivation of latent leukoencephalopathy JC virus infection). Seen in 2–4% of patients with AIDS. Rapidly progressive, usually fatal. Predominantly involves parietal and occipital areas; visual symptoms are common.  risk associated with natalizumab. Other disorders Krabbe disease, metachromatic leukodystrophy, adrenoleukodystrophy. Most common subtype of Guillain-Barré syndrome.


First_Aid_Step1

First_Aid_Step1. Other disorders Krabbe disease, metachromatic leukodystrophy, adrenoleukodystrophy. Most common subtype of Guillain-Barré syndrome. Autoimmune condition that destroys Schwann cells via inflammation and demyelination of motor fibers, sensory fibers, peripheral nerves (including CN III-XII). Likely facilitated by molecular mimicry and triggered by inoculations or stress. Despite association with infections (eg, Campylobacter jejuni, viruses [eg, Zika]), no definitive causal link to any pathogen. Results in symmetric ascending muscle weakness/paralysis and depressed/absent DTRs beginning in lower extremities. Facial paralysis (usually bilateral) and respiratory failure are common. May see autonomic dysregulation (eg, cardiac irregularities, hypertension, hypotension) or sensory abnormalities. Almost all patients survive; majority recover completely after weeks to months. • CSF protein with normal cell count (albuminocytologic dissociation).


First_Aid_Step1

First_Aid_Step1. • CSF protein with normal cell count (albuminocytologic dissociation). Respiratory support is critical until recovery. Disease-modifying treatment: plasmapheresis or IV immunoglobulins. No role for steroids. Congenital nonhereditary anomaly of neural crest derivatives. Somatic mosaicism of an activating mutation in one copy of the GNAQ gene. B  seizures/epilepsy; intellectual disability; episcleral hemangioma  IOP • early-onset glaucoma. Also called encephalotrigeminal angiomatosis. SSTURGGE-Weber: Sporadic, port-wine Stain, Tram track calcifications (opposing gyri), Unilateral, intellectual disability (Retardation), Glaucoma, GNAQ gene, Epilepsy. Tuberous sclerosis AD, variable expression. Mutation in tumor suppressor genes TSC1 on chromosome 9 (hamartin), TSC2 on chromosome 16 (tuberin). Hamartomas in CNS and skin, Angiofibromas


First_Aid_Step1

First_Aid_Step1. Tuberous sclerosis AD, variable expression. Mutation in tumor suppressor genes TSC1 on chromosome 9 (hamartin), TSC2 on chromosome 16 (tuberin). Hamartomas in CNS and skin, Angiofibromas C , Mitral regurgitation, Ash-leaf spots D , cardiac Rhabdomyoma, (Tuberous sclerosis), autosomal dOminant; Mental retardation (intellectual disability), renal Angiomyolipoma E , Seizures, Shagreen patches. HAMARTOMASS.  incidence of Subependymal giant cell astrocytomas and ungual fibromas. AD, 100% penetrance. Mutation in NF1 tumor suppressor gene on chromosome 17 (encodes neurofibromin, a negative RAS regulator). Café-au-lait spots F , Intellectual disability, Cutaneous neurofibromas G , Lisch nodules (pigmented iris hamartomas H ), Optic gliomas, Pheochromocytomas, Seizures/focal neurologic Signs (often from meningioma), bone lesions (eg, sphenoid dysplasia). Also called von Recklinghausen disease. 17 letters in “von Recklinghausen.” CICLOPSS. cells D . H .


First_Aid_Step1

First_Aid_Step1. Also called von Recklinghausen disease. 17 letters in “von Recklinghausen.” CICLOPSS. cells D . H . Cingulate (subfalcine) herniation under Can compress anterior cerebral artery. Falx cerebri falx cerebri Uncal transtentorial herniation Uncus = medial temporal lobe. Early herniation compression), contralateral hemiparesis. Late herniation  coma, Kernohan phenomenon (misleading contralateral blown pupil and ipsilateral hemiparesis due to contralateral compression against Kernohan notch). Central/downward transtentorial Caudal displacement of brain stem  rupture of mass hemorrhages. Usually fatal. Cerebellar tonsillar herniation into the Coma and death result when these herniations foramen magnum compress the brain stem. (less muscle mass,  muscle tone,  reflexes, Upper motor neuron = everything up (tone, Reflexes • DTRs, toes) Tone • Fasciculations = muscle twitching Babinski +− Positive Babinski is normal in infants


First_Aid_Step1

First_Aid_Step1. Upper motor neuron = everything up (tone, Reflexes • DTRs, toes) Tone • Fasciculations = muscle twitching Babinski +− Positive Babinski is normal in infants Poliomyelitis Caused by poliovirus (fecal-oral transmission). Replicates in oropharynx and small intestine before spreading via bloodstream to CNS. Infection causes destruction of cells in anterior horn of spinal cord (LMN death). Signs of LMN lesion: asymmetric weakness (vs symmetric weakness in spinal muscular atrophy), hypotonia, flaccid paralysis, fasciculations, hyporeflexia, muscle atrophy. Respiratory muscle involvement leads to respiratory failure. Signs of infection: malaise, headache, fever, nausea, etc. CSF shows  WBCs (lymphocytic pleocytosis) and slight  of protein (with no change in CSF glucose). Virus recovered from stool or throat.


First_Aid_Step1

First_Aid_Step1. Hemisection of spinal cord. Findings: Ipsilateral loss of all sensation at level of lesion Ipsilateral LMN signs (eg, flaccid paralysis) at level of lesion Ipsilateral UMN signs below level of lesion (due to corticospinal tract damage) Ipsilateral loss of proprioception, vibration, light (2-point discrimination) touch, and tactile sense below level of lesion (due to dorsal column damage) Contralateral loss of pain, temperature, and crude (non-discriminative) touch below level of lesion (due to spinothalamic tract damage) If lesion occurs above T1, patient may present with ipsilateral Horner syndrome due to damage of oculosympathetic pathway. Level of lesion Loss of sensation LMN signs Impaired proprioception, vibration, light touch, tactile sense Impaired pain, temperature, crude touch sensation


First_Aid_Step1

First_Aid_Step1. Level of lesion Loss of sensation LMN signs Impaired proprioception, vibration, light touch, tactile sense Impaired pain, temperature, crude touch sensation Autosomal recessive trinucleotide repeat disorder (GAA)n on chromosome 9 in gene that encodes frataxin (iron-binding protein). Leads to impairment in mitochondrial functioning. Degeneration of lateral corticospinal tract (spastic paralysis), spinocerebellar tract (ataxia), dorsal columns ( vibratory sense, proprioception), and dorsal root ganglia (loss of DTRs). Staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, diabetes mellitus, hypertrophic cardiomyopathy (cause of death). Presents in Friedreich is Fratastic (frataxin): he’s your favorite frat brother, always staggering and falling but has a sweet, big heart. B . Ataxic GAAit.


First_Aid_Step1

First_Aid_Step1. B . Ataxic GAAit. CN V motor lesion Jaw deviates toward side of lesion due to unopposed force from the opposite pterygoid muscle. CN X lesion Uvula deviates away from side of lesion. Weak side collapses and uvula points away. CN XI lesion Weakness turning head to contralateral side of lesion (SCM). Shoulder droop on side of lesion (trapezius). The left SCM contracts to help turn the head to the right. CN XII lesion LMN lesion. Tongue deviates toward side of lesion (“lick your wounds”) due to weakened tongue muscles on affected side. Facial nerve lesions Bell palsy is the most common cause of peripheral facial palsy A . Usually develops after HSV reactivation. Treatment: corticosteroids +/– acyclovir. Most patients gradually recover function, but aberrant regeneration can occur. Other causes of peripheral facial palsy include Lyme disease, herpes zoster (Ramsay Hunt syndrome), sarcoidosis, tumors (eg, parotid gland), diabetes mellitus.


First_Aid_Step1

First_Aid_Step1. lesion loCAtion Motor cortex, connection from motor cortex to Facial nucleus, anywhere along CN VII facial nucleus in pons musCles inVolVed Lower muscles of facial expression Upper and lower muscles of facial expression ForeheAd inVolVed? Spared, due to bilateral UMN innervation Affected other symPtoms None Incomplete eye closure (dry eyes, corneal ulceration), hyperacusis, loss of taste sensation to anterior tongue Face area of motor cortex Outer ear Visible portion of ear (pinna), includes auditory canal and tympanic membrane. Transfers sound waves via vibration of tympanic membrane. Middle ear Air-filled space with three bones called the ossicles (malleus, incus, stapes). Ossicles conduct and amplify sound from tympanic membrane to inner ear.


First_Aid_Step1

First_Aid_Step1. Middle ear Air-filled space with three bones called the ossicles (malleus, incus, stapes). Ossicles conduct and amplify sound from tympanic membrane to inner ear. Inner ear Snail-shaped, fluid-filled cochlea. Contains basilar membrane that vibrates 2° to sound waves. Vibration transduced via specialized hair cells  auditory nerve signaling • brain stem. Each frequency leads to vibration at specific location on basilar membrane (tonotopy): Low frequency heard at apex near helicotrema (wide and flexible). High frequency heard best at base of cochlea (thin and rigid). Weber test Tuning fork on vertex of skull Rinne test Tuning fork in front of ear (air conduction, AC), Tuning fork on mastoid process (bone conduction, BC) No localization BC > AC Localizes to una˜ected ear ˜ transmission of all sound AC > BCAC > BC Localizes to a˜ected ear ˜ transmission of background noise Types of hearing loss


First_Aid_Step1

First_Aid_Step1. Types of hearing loss Cholesteatoma Overgrowth of desquamated keratin debris within the middle ear space ( A , arrows); may erode ossicles, mastoid air cells  conductive hearing loss. Often presents with painless otorrhea. Conjunctivitis Inflammation of the conjunctiva  red eye A . Allergic—itchy eyes, bilateral. Bacterial—pus; treat with antibiotics. Viral—most common, often adenovirus; sparse mucous discharge, swollen preauricular node, • lacrimation; self-resolving. Cataract Painless, often bilateral, opacification of lens A , often resulting in glare and  vision, especially at night. Acquired risk factors:  age, smoking, excessive alcohol use, excessive sunlight, prolonged corticosteroid use, diabetes mellitus, trauma, infection. Congenital risk factors: classic galactosemia, galactokinase deficiency, trisomies (13, 18, 21), TORCH infections (eg, rubella), Marfan syndrome, Alport syndrome, myotonic dystrophy, neurofibromatosis 2.


First_Aid_Step1

First_Aid_Step1. Iris Lens Suspended from ciliary body by zonule fbers. Muscular fbers and position. Iris Dilator muscle (α1) Sphincter muscle (M3) Ciliary body Trabecularmeshwork Cornea Sclera Canal of Schlemm Anterior chamber “Angle” of the eye Lens Trabecular outfow (90%) Drainage through trabecular meshwork canal of Schlemm episcleral vasculature agonist (eg, carbachol, pilocarpine) ↓↓↓Uveoscleral outfow (10%) Drainage into uvea and sclera with prostaglandin agonists (eg, latanoprost, bimatoprost) Aqueous humor Posterior chamber Produced by nonpigmented epithelium on ciliary body and carbonic anhydrase inhibitors (eg, acetazolamide) by β-blockers (eg, timolol), α2-agonists (eg, brimonidine), Glaucoma Optic disc atrophy with characteristic cupping (normal A versus thinning of outer rim of optic nerve head B ), usually with elevated intraocular pressure (IOP) and progressive peripheral visual field loss if untreated. Treatment is through pharmacologic or surgical lowering of IOP.


First_Aid_Step1

First_Aid_Step1. Open-angle glaucoma Associated with  age, African-American race, family history. Painless, more common in US. Primary—cause unclear. Secondary—blocked trabecular meshwork from WBCs (eg, uveitis), RBCs (eg, vitreous hemorrhage), retinal elements (eg, retinal detachment). Uveitis Inflammation of uvea; specific name based on location within affected eye. Anterior uveitis: iritis; posterior uveitis: choroiditis and/or retinitis. May have hypopyon (accumulation of pus in anterior chamber A ) or conjunctival redness. Associated with systemic inflammatory disorders (eg, sarcoidosis, rheumatoid arthritis, juvenile idiopathic arthritis, HLA-B27–associated conditions). Degeneration of macula (central area of retina). Causes distortion (metamorphopsia) and eventual loss of central vision (scotomas).


First_Aid_Step1

First_Aid_Step1. Degeneration of macula (central area of retina). Causes distortion (metamorphopsia) and eventual loss of central vision (scotomas). Dry (nonexudative, > 80%)—Deposition of yellowish extracellular material (“Drusen”) in between Bruch membrane and retinal pigment epithelium A with gradual  in vision. Prevent progression with multivitamin and antioxidant supplements. Wet (exudative, 10–15%)—rapid loss of vision due to bleeding 2° to choroidal neovascularization. Treat with anti-VEGF (vascular endothelial growth factor) injections (eg, bevacizumab, ranibizumab). Diabetic retinopathy Retinal damage due to chronic hyperglycemia. Two types: (arrows in A ) and macular edema. Treatment: blood sugar control. Proliferative—chronic hypoxia results in new blood vessel formation with resultant traction on retina • retinal detachment. Treatment: anti-VEGF injections, peripheral retinal photocoagulation, surgery. Hypertensive Retinal damage due to chronic uncontrolled HTN.


First_Aid_Step1

First_Aid_Step1. Hypertensive Retinal damage due to chronic uncontrolled HTN. retinopathy Flame-shaped retinal hemorrhages, arteriovenous nicking, microaneurysms, macular star (exudate, red arrow in A ), cotton-wool spots (blue arrow in A ). Presence of papilledema requires immediate lowering of BP. Associated with  risk of stroke, CAD, kidney disease. Retinal vein occlusion Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis. Retinal hemorrhage and venous engorgement (“blood and thunder appearance”; arrows in A ), edema in affected area. Separation of neurosensory layer of retina (photoreceptor layer with rods and cones) from outermost pigmented epithelium (normally shields excess light, supports retina)  degeneration of photoreceptors  vision loss. May be 2° to retinal breaks, diabetic traction, inflammatory effusions. Visualized on fundoscopy as crinkling of retinal tissue A and changes in vessel direction.


First_Aid_Step1

First_Aid_Step1. Breaks more common in patients with high myopia and/or history of head trauma. Often preceded by posterior vitreous detachment (“flashes” and “floaters”) and eventual monocular loss of vision like a “curtain drawn down.” Surgical emergency. Central retinal artery Acute, painless monocular vision loss. Retina cloudy with attenuated vessels and “cherry-red” spot occlusion at fovea (center of macula) A . Evaluate for embolic source (eg, carotid artery atherosclerosis, cardiac vegetations, patent foramen ovale). Retinitis pigmentosa Inherited progressive retinal degeneration. Nyctalopia (night blindness)  peripheral vision loss. Bone spicule-shaped deposits A . Papilledema Optic disc swelling (usually bilateral) due to  ICP (eg, 2° to mass effect). Enlarged blind spot and elevated optic disc with blurred margins A . Leukocoria Loss (whitening) of the red reflex. Important causes in children include retinoblastoma A , congenital cataract, toxocariasis.


First_Aid_Step1

First_Aid_Step1. Leukocoria Loss (whitening) of the red reflex. Important causes in children include retinoblastoma A , congenital cataract, toxocariasis. Miosis Constriction, parasympathetic: 1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III 2nd neuron: short ciliary nerves to sphincter pupillae muscles Short ciliary nerves shorten the pupil diameter. Pupillary light reflex Light in either retina sends a signal via CN II to pretectal nuclei (dashed lines in image) in midbrain that activates bilateral Edinger-Westphal nuclei; pupils constrict bilaterally (direct and consensual reflex). Result: illumination of 1 eye results in bilateral pupillary constriction.


First_Aid_Step1

First_Aid_Step1. Mydriasis Dilation, sympathetic: 1st neuron: hypothalamus to ciliospinal center of Budge (C8–T2) 2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels) 3rd neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles. Sympathetic fibers also innervate smooth muscle of eyelids (minor retractors) and sweat glands of forehead and face. Long ciliary nerves make the pupil diameter longer. Marcus Gunn pupil Also called relative afferent pupillary defect (RAPD). When the light shines into a normal eye, constriction of the ipsilateral (direct reflex) and contralateral eye (consensual reflex) is observed. When the light is then swung to the affected eye, both pupils dilate instead of constrict due to impaired conduction of light signal along the injured optic nerve. Associated with optic neuritis, early multiple sclerosis.


First_Aid_Step1

First_Aid_Step1. Sympathetic denervation of face : PAM is horny (Horner).  Ptosis (slight drooping of eyelid: superior Hypothalamus Ophthalmic divisiontarsal muscle) of trigeminal nerve Anhidrosis (absence of sweating) and Long ciliary nerve flushing of affected side of face To sweat glands of forehead To smooth muscle of eyelid Associated with lesions along the sympathetic chain: Internal carotid To sweat glands of face  1st neuron: pontine hemorrhage, lateral artery medullary syndrome, spinal cord lesion Third neuron above T1 (eg, Brown-Séquard syndrome, First neuron 2nd neuron: stellate ganglion compression lateral horn 3rd neuron: carotid dissection (painful) Spinal cord Superior Superior Superior CN VI innervates the Lateral Rectus. oblique rectus oblique CN IV innervates the Superior Oblique. CN III innervates the Rest. Medial rectus The “chemical formula” LR6SO4R3. muscle Obliques go Opposite (left SO and IO tested with patient looking right). IOU: IO tested looking Up.


First_Aid_Step1

First_Aid_Step1. CN III innervates the Rest. Medial rectus The “chemical formula” LR6SO4R3. muscle Obliques go Opposite (left SO and IO tested with patient looking right). IOU: IO tested looking Up. CN III, IV, VI palsies CN III damage CN III has both motor (central) and parasympathetic (peripheral) components. Common causes include: Cavernous sinus thrombosis • proptosis, involvement of CNs IV, V1/V2, VI Motor output to extraocular muscles—affected primarily by vascular disease (eg, diabetes mellitus: glucose  sorbitol) due to  diffusion of oxygen and nutrients to the interior fibers from compromised vasculature that resides on outside of nerve. Signs: ptosis, “down-and-out” gaze. Parasympathetic output—fibers on the periphery are first affected by compression (eg, PCom aneurysm, uncal herniation). Signs: diminished or absent pupillary light reflex, “blown pupil” often with “down-and-out” gaze A .


First_Aid_Step1

First_Aid_Step1. A . Visual field defects 1. Right anopia (monocular vision loss) 4Opticchiasm7 Macula Opticnerve Optic tractVisual 13 52Dorsal optic radiation(parietallobe)Lt. Rt.Lateralgeniculatebody Defect in visual feld of L eye R eye 2. Bitemporal hemianopia (pituitary lesion, chiasm) 3. 4. Left upper quadrantanopia (right temporal lesion, MCA) 5. loop(right parietal lesion, MCA) (temporal 6. Left hemianopia with macular sparing (right occipital lesion, PCA) 7. Central scotoma (eg, macular degeneration) PCA infarct) 6 Calcarine cortex sulcus Meyer Loop—Lower retina; Loops around inferior horn of Lateral ventricle. Note: When an image hits 1° visual cortex, it is upsideDorsal optic radiation—superior retina; takes down and left-right reversed. shortest path via internal capsule.


First_Aid_Step1

First_Aid_Step1. Note: When an image hits 1° visual cortex, it is upsideDorsal optic radiation—superior retina; takes down and left-right reversed. shortest path via internal capsule. Cavernous sinus Collection of venous sinuses on either side of pituitary. Blood from eye and superficial cortex  cavernous sinus  internal jugular vein. CNs III, IV, V1, V2, and VI plus postganglionic sympathetic pupillary fibers en route to orbit all pass through cavernous sinus. Cavernous portion of internal carotid artery is also here. Cavernous sinus syndrome—presents with variable ophthalmoplegia,  corneal sensation, Horner syndrome and occasional decreased maxillary sensation. 2° to pituitary tumor mass effect, carotid-cavernous fistula, or cavernous sinus thrombosis related to infection.


First_Aid_Step1

First_Aid_Step1. 3rd ventricle Oculomotor n. (CN III) Trochlear n. (CN IV) Ophthalmic n. (CN V1) Optic chiasma (CN II) Maxillary n. (CN V2) Pituitary Pia Dura Arachnoid Sphenoid sinus Subarachnoid space Anterior cerebral a. Internal carotid a. Cavernous sinus Abducens n. (CN VI) Medial longitudinal fasciculus (MLF): pair of tracts that allows for crosstalk between CN VI and CN III nuclei. Coordinates both eyes to move in same horizontal direction. Highly myelinated (must communicate quickly so eyes move at same time). Lesions may be unilateral or bilateral (latter classically seen in multiple sclerosis, stroke). Lesion in MLF = internuclear ophthalmoplegia (INO), a conjugate horizontal gaze palsy. Lack of communication such that when CN VI nucleus activates ipsilateral lateral rectus, contralateral CN III nucleus does not stimulate medial rectus to contract. Abducting eye displays nystagmus (CN VI overfires to stimulate CN III). Convergence normal. MLF in MS.


First_Aid_Step1

First_Aid_Step1. MLF in MS. When looking left, the left nucleus of CN VI fires, which contracts the left lateral rectus and stimulates the contralateral (right) nucleus of CN III via the right MLF to contract the right medial rectus. Directional term (eg, right INO, left INO) refers to the eye that is unable to adduct. INO = Ipsilateral adduction failure, Nystagmus Opposite. Sedation, tolerance, Also for eclampsia seizures (1st dependence, respiratory line is MgSO4) depression Diplopia, ataxia, blood 1st line for trigeminal neuralgia dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis (cleft lip/palate, spina bifida), induction of cytochrome P-450, SIADH, SJS Sucks to have Silent causes Fatigue, GI distress, (absence) Seizures Headache, Itching (and urticaria), SJS


First_Aid_Step1

First_Aid_Step1. Sucks to have Silent causes Fatigue, GI distress, (absence) Seizures Headache, Itching (and urticaria), SJS PHENYTOIN: cytochrome P-450 induction, Hirsutism, Enlarged gums, Nystagmus, Yellow-brown skin, Teratogenicity (fetal hydantoin syndrome), Osteopenia, Inhibited folate absorption, Neuropathy. Rare: SJS, DRESS syndrome, SLE-like syndrome. Toxicity leads to diplopia, ataxia, sedation. Sedation, slow cognition, Also used for migraine kidney stones, skinny (weight prophylaxis loss), sight threatened (glaucoma), speech (wordfinding) difficulties GI distress, rare but fatal Also used for myoclonic seizures, bipolar disorder, hepatotoxicity (measure migraine prophylaxis LFTs), pancreatitis, neural tube defects, tremor, weight gain, contraindicated in Vision gone all bad with  GABA. Irreversible GABA * = Common use, ** = 1st line for acute, *** = 1st line for recurrent seizure prophylaxis. Barbiturates Phenobarbital, pentobarbital, thiopental, secobarbital.


First_Aid_Step1

First_Aid_Step1. Barbiturates Phenobarbital, pentobarbital, thiopental, secobarbital. meChAnism Facilitate GABAA action by • duration of Cl− channel opening, thus  neuron firing (barbidurates • duration). CliniCAl use Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental). AdVerse eFFeCts Respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by alcohol use); dependence; drug interactions (induces cytochrome P-450). Overdose treatment is supportive (assist respiration and maintain BP). Contraindicated in porphyria. Benzodiazepines Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam. meChAnism Facilitate GABAA action by • frequency of Cl– channel opening (“frenzodiazepines” • frequency).  REM sleep. Most have long half-lives and active metabolites (exceptions [ATOM]: Alprazolam, Triazolam, Oxazepam, and Midazolam are short acting  higher addictive potential).


First_Aid_Step1

First_Aid_Step1.  REM sleep. Most have long half-lives and active metabolites (exceptions [ATOM]: Alprazolam, Triazolam, Oxazepam, and Midazolam are short acting  higher addictive potential). CliniCAl use Anxiety, panic disorder, spasticity, status epilepticus (lorazepam, diazepam, midazolam), eclampsia, detoxification (especially alcohol withdrawal– DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia). Lorazepam, Oxazepam, and Temazepam can be used for those with liver disease who drink a LOT due to minimal first-pass metabolism. AdVerse eFFeCts Dependence, additive CNS depression effects with alcohol and barbiturates (all bind the GABAA receptor). Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor). Can precipitate seizures by causing acute benzodiazepine withdrawal.


First_Aid_Step1

First_Aid_Step1. Nonbenzodiazepine Zolpidem, Zaleplon, esZopiclone. “These ZZZs put you to sleep.” hypnotics meChAnism Act via the BZ1 subtype of the GABA receptor. Effects reversed by flumazenil. Sleep cycle less affected as compared with benzodiazepine hypnotics. CliniCAl use Insomnia. AdVerse eFFeCts Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects.  dependence risk than benzodiazepines. meChAnism Orexin (hypocretin) receptor antagonist. Suvorexant is an orexin antagonist. CliniCAl use Insomnia. AdVerse eFFeCts CNS depression (somnolence), headache, abnormal sleep-related activities. Contraindications: narcolepsy, combination with strong CYP3A4 inhibitors. Not recommended in patients with liver disease. Limited physical dependence or abuse potential.


First_Aid_Step1

First_Aid_Step1. AdVerse eFFeCts Dizziness, nausea, fatigue, headache. No dependence (not a controlled substance). meChAnism 5-HT agonists. Inhibit trigeminal nerve A sumo wrestler trips and falls on his head. activation, prevent vasoactive peptide release, induce vasoconstriction. CliniCAl use Acute migraine, cluster headache attacks. AdVerse eFFeCts Coronary vasospasm (contraindicated in patients with CAD or vasospastic angina), mild paresthesia, serotonin syndrome (in combination with other 5-HT agonists). meChAnism • dopamine in brain. Unlike dopamine, l-DOPA can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine. Carbidopa, a peripheral DOPA decarboxylase inhibitor, is given with l-DOPA to  bioavailability of l-DOPA in the brain and to limit peripheral side effects. CliniCAl use Parkinson disease.


First_Aid_Step1

First_Aid_Step1. CliniCAl use Parkinson disease. AdVerse eFFeCts Nausea, hallucinations, postural hypotension. With progressive disease, l-DOPA can lead to “onoff” phenomenon with improved mobility during “on” periods, then impaired motor function during “off” periods when patient responds poorly to l-DOPA or medication wears off. Selegiline, rasagiline meChAnism Selectively inhibit MAO-B (metabolize dopamine) • dopamine availability. Selegiline selectively inhibits MAO-B and is more commonly found in the Brain than in the periphery. CliniCAl use Adjunctive agent to l-DOPA in treatment of Parkinson disease. AdVerse eFFeCts May enhance adverse effects of l-DOPA. Inhaled anesthetics Desflurane, halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, N2O. meChAnism Mechanism unknown. eFFeCts Myocardial depression, respiratory depression, postoperative nausea/vomiting,  cerebral blood flow,  cerebral metabolic demand.


First_Aid_Step1

First_Aid_Step1. meChAnism Mechanism unknown. eFFeCts Myocardial depression, respiratory depression, postoperative nausea/vomiting,  cerebral blood flow,  cerebral metabolic demand. AdVerse eFFeCts Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane, epileptogenic), expansion of trapped gas in a body cavity (N2O). Malignant hyperthermia—rare, life-threatening condition in which inhaled anesthetics or succinylcholine induce severe muscle contractions and hyperthermia. Susceptibility is often inherited as autosomal dominant with variable penetrance. Mutations in voltage-sensitive ryanodine receptor (RYR1 gene) cause • Ca2+ release from sarcoplasmic reticulum. Treatment: dantrolene (a ryanodine receptor antagonist). Local anesthetics Esters—procaine, tetracaine, benzocaine, chloroprocaine. Amides—lIdocaIne, mepIvacaIne, bupIvacaIne, ropIvacaIne (amIdes have 2 I’s in name).


First_Aid_Step1

First_Aid_Step1. Local anesthetics Esters—procaine, tetracaine, benzocaine, chloroprocaine. Amides—lIdocaIne, mepIvacaIne, bupIvacaIne, ropIvacaIne (amIdes have 2 I’s in name). meChAnism Block Na+ channels by binding to specific receptors on inner portion of channel. Most effective in rapidly firing neurons. 3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form. Can be given with vasoconstrictors (usually epinephrine) to enhance local action— bleeding,  anesthesia by  systemic concentration. In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively  need more anesthetic. Order of nerve blockade: small-diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers.


First_Aid_Step1

First_Aid_Step1. Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure. CliniCAl use Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides. AdVerse eFFeCts CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, arrhythmias (cocaine), methemoglobinemia (benzocaine). Spasmolytics, antispasmodics meChAnism Act as agonists at opioid receptors (μ = β-endorphin, δ = enkephalin, κ = dynorphin) to modulate synaptic transmission—close presynaptic Ca2+ channels, open postsynaptic K+ channels  synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P. eFFiCACy Full agonist: morphine, heroin, meperidine, methadone, codeine, fentanyl. Partial agonist: buprenorphine. Mixed agonist/antagonist: nalbuphine, pentazocine, butorphanol. Antagonist: naloxone, naltrexone, methylnaltrexone.


First_Aid_Step1

First_Aid_Step1. CliniCAl use Moderate to severe or refractory pain, diarrhea (loperamide, diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (methadone, buprenorphine + naloxone). AdVerse eFFeCts Nausea, vomiting, pruritus, addiction, respiratory depression, constipation, sphincter of Oddi spasm, miosis (except meperidine  mydriasis), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Treat toxicity with naloxone (competitive opioid receptor antagonist) and prevent relapse with naltrexone once detoxified. meChAnism Very weak opioid agonist; also inhibits the Tramadol is a Slight opioid agonist, and a reuptake of norepinephrine and serotonin. Serotonin and norepinephrine reuptake inhibitor. It is used for Stubborn pain, but CliniCAl use Chronic pain. can lower Seizure threshold, and may cause AdVerse eFFeCts Similar to opioids; decreases seizure threshold; Serotonin Syndrome. serotonin syndrome.


First_Aid_Step1

First_Aid_Step1. CliniCAl use Chronic pain. can lower Seizure threshold, and may cause AdVerse eFFeCts Similar to opioids; decreases seizure threshold; Serotonin Syndrome. serotonin syndrome. Glaucoma therapy  IOP via  amount of aqueous humor (inhibit synthesis/secretion or • drainage). BAD humor may not be Politically Correct. β-blockers Timolol, betaxolol, carteolol  aqueous humor synthesis No pupillary or vision changes α-agonists Epinephrine (α1),  aqueous humor synthesis via Mydriasis (α1); do not use in apraclonidine, vasoconstriction (epinephrine) closed-angle glaucoma brimonidine (α2)  aqueous humor synthesis Blurry vision, ocular (apraclonidine, brimonidine) hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus Diuretics Acetazolamide  aqueous humor synthesis No pupillary or vision changes via inhibition of carbonic anhydrase


First_Aid_Step1

First_Aid_Step1. Diuretics Acetazolamide  aqueous humor synthesis No pupillary or vision changes via inhibition of carbonic anhydrase Prostaglandins Bimatoprost, latanoprost  outflow of aqueous humor via Darkens color of iris (PGF2α)  resistance of flow through (browning), eyelash growth uveoscleral pathway


First_Aid_Step1

First_Aid_Step1. Prostaglandins Bimatoprost, latanoprost  outflow of aqueous humor via Darkens color of iris (PGF2α)  resistance of flow through (browning), eyelash growth uveoscleral pathway Cholinomimetics (M3) Direct: pilocarpine, carbachol  outflow of aqueous humor via Miosis (contraction of pupillary Indirect: physostigmine, contraction of ciliary muscle sphincter muscles) and echothiophate and opening of trabecular cyclospasm (contraction of meshwork ciliary muscle) Use pilocarpine in acute angle closure glaucoma—very effective at opening meshwork into canal of Schlemm “Words of comfort, skillfully administered, are the oldest therapy known to man.” “All men should strive to learn before they die what they are running from, and to, and why.” “The sorrow which has no vent in tears may make other organs weep.” “It’s no use going back to yesterday, because I was a different person then.” —Lewis Carroll, Alice in Wonderland


First_Aid_Step1

First_Aid_Step1. This chapter encompasses overlapping areas in psychiatry, psychology, sociology, and psychopharmacology. High-yield topics include schizophrenia, mood disorders, eating disorders, personality disorders, somatic symptom disorders, substance abuse, and antipsychotic agents. Know the DSM-5 criteria for diagnosing common psychiatric disorders. Operant conditioning Learning in which a particular action is elicited because it produces a punishment or reward. Usually elicits voluntary responses. Reinforcement Target behavior (response) is followed by desired Skinner operant conditioning quadrants: reward (positive reinforcement) or removal of aversive stimulus (negative reinforcement). Punishment Repeated application of aversive stimulus (positive punishment) or removal of desired reward (negative punishment) to extinguish unwanted behavior. Extinction Discontinuation of reinforcement (positive or negative) eventually eliminates behavior. Can occur in operant or classical conditioning.


First_Aid_Step1

First_Aid_Step1. Extinction Discontinuation of reinforcement (positive or negative) eventually eliminates behavior. Can occur in operant or classical conditioning. Transference Patient projects feelings about formative or other important persons onto physician (eg, psychiatrist is seen as parent). Countertransference Doctor projects feelings about formative or other important persons onto patient (eg, patient reminds physician of younger sibling). Ego defenses Thoughts and behaviors (voluntary or involuntary) used to resolve conflict and prevent undesirable feelings (eg, anxiety, depression). Denial Avoiding the awareness of some painful reality. A patient with cancer plans a full-time work schedule despite being warned of significant fatigue during chemotherapy. Mature adults wear a SASH. Lack of basic trust Reactive attachment disorder (infant withdrawn/unresponsive to comfort) Disinhibited social engagement (child indiscriminately attaches to strangers)


First_Aid_Step1

First_Aid_Step1. Lack of basic trust Reactive attachment disorder (infant withdrawn/unresponsive to comfort) Disinhibited social engagement (child indiscriminately attaches to strangers) Child neglect Failure to provide a child with adequate food, shelter, supervision, education, and/or affection. Most common form of child maltreatment. Signs: poor hygiene, malnutrition, withdrawal, impaired social/emotional development, failure to thrive. As with child abuse, suspected child neglect must be reported to local child protective services.


First_Aid_Step1

First_Aid_Step1. Onset before age 12. ≥ 6 months of limited attention span and/or poor impulse control. Characterized by hyperactivity, impulsivity, and/or inattention in ≥ 2 settings (eg, school, home, places of worship). Normal intelligence, but commonly coexists with difficulties in school. Often persists into adulthood. Commonly coexists with oppositional defiant disorder. Treatment: stimulants (eg, methylphenidate) +/– behavioral therapy; alternatives include atomoxetine, guanfacine, clonidine. Conduct disorder Repetitive, pervasive behavior violating societal norms or the basic rights of others (eg, aggression toward people and animals, destruction of property, theft). After age 18, often reclassified as antisocial personality disorder. Treatment: psychotherapy (eg, cognitive behavioral therapy [CBT]).


First_Aid_Step1

First_Aid_Step1. Intellectual disability Global cognitive deficits (vs specific learning disorder) that affect reasoning, memory, abstract thinking, judgment, language, learning. Adaptive functioning is impaired, leading to major difficulties with education, employment, communication, socialization, independence. Treatment: psychotherapy, occupational therapy, special education. Oppositional defiant Enduring pattern of anger and irritability with argumentative, vindictive, and defiant behavior disorder toward authority figures. Treatment: psychotherapy (eg, CBT). Selective mutism Onset before age 5. Anxiety disorder lasting ≥ 1 month involving refraining from speech in certain situations despite speaking in other, usually more comfortable situations. Development (eg, speech and language) not typically impaired. Interferes with social, academic, and occupational tasks. Commonly coexists with social anxiety disorder. Treatment: behavioral, family, and play therapy; SSRIs.


First_Aid_Step1

First_Aid_Step1. Tourette syndrome Onset before age 18. Sudden, Sudden, recurrent, nonrhythmic, stereotyped motor and vocal tics that persist for > 1 year. Coprolalia (involuntary obscene speech) found in some patients. Associated with OCD and ADHD. Treatment: psychoeducation, behavioral therapy. For intractable and distressing tics, high-potency antipsychotics (eg, haloperidol, fluphenazine), tetrabenazine, α2-agonists (eg, guanfacine, clonidine), or atypical antipsychotics. Orientation Patients’ ability to know the date and time, where they are, and who they are (order of loss: time  place  person). Common causes of loss of orientation: alcohol, drugs, fluid/electrolyte imbalance, head trauma, hypoglycemia, infection, nutritional deficiencies, hypoxia. Depersonalization/ Persistent feelings of detachment or estrangement from one’s own body, thoughts, perceptions, derealization and actions (depersonalization) or one’s environment (derealization). Intact reality testing (vs disorder psychosis).


First_Aid_Step1

First_Aid_Step1. Delirium “Waxing and waning” level of consciousness with acute onset,  attention span,  level of arousal. Characterized by disorganized thinking, hallucinations (often visual), misperceptions (eg, illusions), disturbance in sleep-wake cycle, cognitive dysfunction, agitation. Reversible. Usually 2° to other identifiable illness (eg, CNS disease, infection, trauma, substance abuse/ withdrawal, metabolic/electrolyte disturbances, hemorrhage, urinary/fecal retention), or medications (eg, anticholinergics), especially in the elderly. Most common presentation of altered mental status in inpatient setting, especially in the ICU or during prolonged hospital stays. EEG may show diffuse background rhythm slowing. Delirium = changes in sensorium.


First_Aid_Step1

First_Aid_Step1. Delirium = changes in sensorium. Treatment: identification and management of underlying condition. Orientation protocols (eg, keeping a clock or calendar nearby),  sleep disturbances, and  cognitive stimulation to manage symptoms. Antipsychotics as needed. Avoid unnecessary restraints and drugs that may worsen delirium (eg, anticholinergics, benzodiazepines, opioids). Psychosis Distorted perception of reality characterized by delusions, hallucinations, and/or disorganized thought/speech. Can occur in patients with medical illness, psychiatric illness, or both. Delusions False, fixed, idiosyncratic beliefs that persist despite evidence to the contrary and are not typical of a patient’s culture or religion (eg, a patient who believes that others are reading his thoughts). Types include erotomanic, grandiose, jealous, persecutory, somatic, mixed, and unspecified. Disorganized thought Speech may be incoherent (“word salad”), tangential, or derailed (“loose associations”).


First_Aid_Step1

First_Aid_Step1. Disorganized thought Speech may be incoherent (“word salad”), tangential, or derailed (“loose associations”). Hallucinations Perceptions in the absence of external stimuli (eg, seeing a light that is not actually present). Contrast with misperceptions (eg, illusions) of real external stimuli. Types include: Auditory—more commonly due to psychiatric illness (eg, schizophrenia) than medical illness. Visual—more commonly due to medical illness (eg, drug intoxication, delirium) than psychiatric illness. Tactile—common in alcohol withdrawal and stimulant use (eg, “cocaine crawlies,” a type of delusional parasitosis). Olfactory—often occur as an aura of temporal lobe epilepsy (eg, burning rubber) and in brain tumors. Gustatory—rare, but seen in epilepsy. Hypnagogic—occurs while going to sleep. Sometimes seen in narcolepsy. Hypnopompic—occurs while waking from sleep (“get pomped up in the morning”). Sometimes seen in narcolepsy.


First_Aid_Step1

First_Aid_Step1. Hypnagogic—occurs while going to sleep. Sometimes seen in narcolepsy. Hypnopompic—occurs while waking from sleep (“get pomped up in the morning”). Sometimes seen in narcolepsy. Schizophrenia Chronic illness causing profound functional impairment. Symptom categories include: Positive—hallucinations, delusions, unusual thought processes, disorganized speech, bizarre behavior Negative—flat or blunted affect, apathy, anhedonia, alogia, social withdrawal Cognitive—reduced ability to understand or make plans, diminished working memory, inattention Diagnosis requires ≥ 2 of the following active symptoms, including ≥ 1 from symptoms #1–3: 1. 2. Hallucinations, often auditory 3. 4. 5. Requires ≥ 1 month of active symptoms over the past 6 months; onset ≥ 6 months prior to diagnosis.


First_Aid_Step1

First_Aid_Step1. 2. Hallucinations, often auditory 3. 4. 5. Requires ≥ 1 month of active symptoms over the past 6 months; onset ≥ 6 months prior to diagnosis. Associated with altered dopaminergic activity,  serotonergic activity, and  dendritic branching. Ventriculomegaly on brain imaging. Lifetime prevalence—1.5% (males > females). Presents earlier in men (late teens to early 20s) than in women (late 20s to early 30s).  suicide risk. Heavy cannabis use in adolescence is associated with  incidence and worsened course of psychotic, mood, and anxiety disorders. Treatment: atypical antipsychotics (eg, risperidone) are first line. Negative symptoms often persist after treatment, despite resolution of positive symptoms. Brief psychotic disorder—≥ 1 positive symptom(s) lasting < 1 month, usually stress-related. Schizophreniform disorder—≥ 2 symptoms lasting 1–6 months.


First_Aid_Step1

First_Aid_Step1. Brief psychotic disorder—≥ 1 positive symptom(s) lasting < 1 month, usually stress-related. Schizophreniform disorder—≥ 2 symptoms lasting 1–6 months. Schizoaffective Shares symptoms with both schizophrenia and mood disorders (major depressive or bipolar disorder disorder). To differentiate from a mood disorder with psychotic features, patient must have > 2 weeks of psychotic symptoms without a manic or depressive episode. Delusional disorder ≥ 1 delusion(s) lasting > 1 month, but without a mood disorder or other psychotic symptoms. Daily functioning, including socialization, may be impacted by the pathological, fixed belief but is otherwise unaffected. Can be shared by individuals in close relationships (folie à deux). Schizotypal personality Cluster A personality disorder that also falls on the schizophrenia spectrum. May include brief disorder psychotic episodes (eg, delusions) that are less frequent and severe than in schizophrenia.


First_Aid_Step1

First_Aid_Step1. Mood disorder Characterized by an abnormal range of moods or internal emotional states and loss of control over them. Severity of moods causes distress and impairment in social and occupational functioning. Includes major depressive, bipolar, dysthymic, and cyclothymic disorders. Episodic superimposed psychotic features (delusions, hallucinations, disorganized speech/behavior) may be present. Manic episode Distinct period of abnormally and persistently elevated, expansive, or irritable mood and  activity or energy lasting ≥ 1 week. Diagnosis requires hospitalization or marked functional impairment with ≥ 3 of the following (manics DIG FAST): Distractibility • Flight of ideas—racing thoughts Impulsivity/Indiscretion—seeks pleasure •  goal-directed Activity/psychomotor without regard to consequences (hedonistic) Agitation


First_Aid_Step1

First_Aid_Step1. Distractibility • Flight of ideas—racing thoughts Impulsivity/Indiscretion—seeks pleasure •  goal-directed Activity/psychomotor without regard to consequences (hedonistic) Agitation Hypomanic episode Similar to a manic episode except mood disturbance is not severe enough to cause marked impairment in social and/or occupational functioning or to necessitate hospitalization. Abnormally  activity or energy usually present. No psychotic features. Lasts ≥ 4 consecutive days. length of time). Bipolar II—a hypomanic and a depressive episode (no history of manic episodes). Patient’s mood and functioning usually normalize between episodes. Use of antidepressants can destabilize mood. High suicide risk. Treatment: mood stabilizers (eg, lithium, valproic acid, carbamazepine, lamotrigine), atypical antipsychotics.


First_Aid_Step1

First_Aid_Step1. Cyclothymic disorder—milder form of bipolar disorder fluctuating between mild depressive and hypomanic symptoms. Must last ≥ 2 years with symptoms present at least half of the time, with any remission lasting ≤ 2 months. Recurrent episodes lasting ≥ 2 weeks characterized by ≥ 5 of 9 diagnostic symptoms (must include depressed mood or anhedonia) (DIGS SPACE): Guilt or feelings of worthlessness Screen for previous manic or hypomanic episodes to rule out bipolar disorder. Treatment: CBT and SSRIs are first line. Also SNRIs, mirtazapine, bupropion, electroconvulsive therapy (ECT). Persistent depressive Often milder than MDD; ≥ 2 depressive symptoms lasting ≥ 2 years (≥ 1 year in children), with any disorder (dysthymia) remission lasting ≤ 2 months.


First_Aid_Step1

First_Aid_Step1. Persistent depressive Often milder than MDD; ≥ 2 depressive symptoms lasting ≥ 2 years (≥ 1 year in children), with any disorder (dysthymia) remission lasting ≤ 2 months. MDD with seasonal Formerly called seasonal affective disorder. Major depressive episodes occurring only during a pattern particular season (usually winter) in ≥ 2 consecutive years and in most years across a lifetime. Atypical symptoms common. Depression with atypical features Characterized by mood reactivity (transient improvement in response to a positive event), hypersomnia, hyperphagia, leaden paralysis (heavy feeling in arms and legs), long-standing interpersonal rejection sensitivity. Most common subtype of depression. Treatment: CBT and SSRIs are first line. MAO inhibitors (MAOIs) are effective but not first line because of their risk profile.


First_Aid_Step1

First_Aid_Step1. MDD with peripartum 10–15% incidence rate. Formerly called postpartum depression. Meets MDD criteria with onset no onset later than 1 year after delivery. Treatment: CBT and SSRIs are first line. Postpartum psychosis 0.1–0.2% incidence rate. Characterized by mood-congruent delusions, hallucinations, and thoughts of harming the baby or self. Risk factors include first pregnancy, family history, bipolar disorder, psychotic disorder, recent medication change. Treatment: hospitalization and initiation of atypical antipsychotic; if insufficient, ECT may be used.


First_Aid_Step1

First_Aid_Step1. Grief The five stages of grief per the Kübler-Ross model are denial, anger, bargaining, depression, and acceptance (may occur in any order). Other normal grief symptoms include shock, guilt, sadness, anxiety, yearning, and somatic symptoms that usually occur in waves. Simple hallucinations of the deceased person are common (eg, hearing the deceased speaking). Any thoughts of dying are limited to joining the deceased (vs complicated grief). Duration varies widely; usually resolves within 6–12 months. Persistent complex bereavement disorder involves obsessive preoccupation with the deceased and causes functional impairment, lasting at least 12 months (6 months in children). Can also meet criteria for major depressive episode. SAD PERSONS are more likely to complete suicide. Most common method in US is firearms; access to guns  risk of suicide completion. Women try more often; men complete more often.


First_Aid_Step1

First_Aid_Step1. SAD PERSONS are more likely to complete suicide. Most common method in US is firearms; access to guns  risk of suicide completion. Women try more often; men complete more often. Other risk factors include recent psychiatric hospitalization and family history of completed suicide. Anxiety disorders Inappropriate experiences of fear/worry and their physical manifestations incongruent with the magnitude of the stressors. Symptoms are not attributable to another psychiatric disorder, medical condition (eg, hyperthyroidism), or substance abuse. Includes panic disorder, phobias, generalized anxiety disorder, and selective mutism. Phobias Severe, persistent (≥ 6 months) fear or anxiety due to presence or anticipation of a specific object or situation. Person often recognizes fear is excessive. Treatment: CBT with exposure therapy.


First_Aid_Step1

First_Aid_Step1. Social anxiety disorder—exaggerated fear of embarrassment in social situations (eg, public speaking, using public restrooms). Treatment: CBT, SSRIs, venlafaxine. For performance type (eg, anxiety restricted to public speaking), use β-blockers or benzodiazepines as needed. Agoraphobia—irrational fear/anxiety while facing or anticipating ≥ 2 specific situations (eg, open/ closed spaces, lines, crowds, public transport). If severe, patients may refuse to leave their homes. Associated with panic disorder. Treatment: CBT, SSRIs. Trichotillomania Compulsively pulling out one’s hair. Causes significant distress and persists despite attempts to stop. Presents with areas of thinning hair or baldness on any area of the body, most commonly the scalp A . Incidence highest in childhood but spans all ages. Treatment: psychotherapy.


First_Aid_Step1

First_Aid_Step1. A . Incidence highest in childhood but spans all ages. Treatment: psychotherapy. Adjustment disorder Emotional or behavioral symptoms (eg, anxiety, outbursts) that occur within 3 months of an identifiable psychosocial stressor (eg, divorce, illness) lasting < 6 months once the stressor has ended. If symptoms persist > 6 months after stressor ends, it is GAD. Symptoms do not meet criteria for MDD. Treatment: CBT is first line; antidepressants and anxiolytics may be considered. Schizoid Voluntary social withdrawal (Aloof), limited emotional expression, content with social isolation (vs avoidant). Factitious disorders Symptoms are intentional, motivation is unconscious. Patient consciously creates physical and/or psychological symptoms in order to assume “sick role” and to get medical attention and sympathy (1° [internal] gain).


First_Aid_Step1

First_Aid_Step1. Conversion disorder Also called functional neurologic symptom disorder. Loss of sensory or motor function (eg, paralysis, blindness, mutism), often following an acute stressor; patient may be aware of but indifferent toward symptoms (la belle indifférence); more common in females, adolescents, and young adults. Illness anxiety Preoccupation with acquiring or having a serious illness, often despite medical evaluation and disorder reassurance; minimal to no somatic symptoms.


First_Aid_Step1

First_Aid_Step1. Illness anxiety Preoccupation with acquiring or having a serious illness, often despite medical evaluation and disorder reassurance; minimal to no somatic symptoms. Bulimia nervosa Recurring episodes of binge eating with compensatory purging behaviors at least weekly over the last 3 months. BMI often normal or slightly overweight (vs anorexia). Associated with parotid gland hypertrophy (may see • serum amylase), enamel erosion, Mallory-Weiss syndrome, electrolyte disturbances (eg,  K+ , • Cl−), metabolic alkalosis, dorsal hand calluses from induced vomiting (Russell sign). Treatment: psychotherapy, nutritional rehabilitation, antidepressants (eg, SSRIs). Bupropion is contraindicated due to seizure risk.


First_Aid_Step1

First_Aid_Step1. Sleep terror disorder Periods of inconsolable terror with screaming in the middle of the night. Most common in children. Occurs during slow-wave/deep (stage N3) non-REM sleep with no memory of the arousal episode, as opposed to nightmares that occur during REM sleep (remembering a scary dream). Triggers include emotional stress, fever, and lack of sleep. Usually self limited. Enuresis Nighttime urinary incontinence ≥ 2 times/week for ≥ 3 months in person > 5 years old. First-line treatment: behavioral modification (eg, scheduled voids, nighttime fluid restriction) and positive reinforcement. For refractory cases: bedwetting alarm, oral desmopressin (ADH analog; preferred over imipramine due to fewer side effects).


First_Aid_Step1

First_Aid_Step1. Narcolepsy Excessive daytime sleepiness (despite awakening well-rested) with recurrent episodes of rapid-onset, overwhelming sleepiness ≥ 3 times/week for the last 3 months. Due to • orexin (hypocretin) production in lateral hypothalamus and dysregulated sleep-wake cycles. Associated with: Hypnagogic (just before going to sleep) or hypnopompic (just before awakening; get pomped up in the morning) hallucinations. Nocturnal and narcoleptic sleep episodes that start with REM sleep (sleep paralysis). Cataplexy (loss of all muscle tone following strong emotional stimulus, such as laughter). Treatment: good sleep hygiene (scheduled naps, regular sleep schedule), daytime stimulants (eg, amphetamines, modafinil) and/or nighttime sodium oxybate (GHB). Stages of change in overcoming addiction Maladaptive pattern of substance use involving ≥ 2 of the following in the past year: Intense, distracting cravings Using more, or longer, than intended


First_Aid_Step1

First_Aid_Step1. Stages of change in overcoming addiction Maladaptive pattern of substance use involving ≥ 2 of the following in the past year: Intense, distracting cravings Using more, or longer, than intended Persistent desire but inability to cut down Time-consuming substance acquisition, use, or recovery Impaired functioning at work, school, or home > 1 episode of use involving danger (eg, unsafe sex, driving while impaired) Continued use despite awareness of harm 1. 2. Contemplation—acknowledging problem, but unwilling to change 3. 4. 5. 6. Relapse—(if applicable) returning to old behaviors and abandoning changes Nonspecific: mood elevation,  anxiety, sedation, Nonspecific: anxiety, tremor, seizures, behavioral disinhibition, respiratory depression. insomnia. Alcohol Emotional lability, slurred speech, ataxia, coma, blackouts. Serum γ-glutamyltransferase (GGT)—sensitive indicator of alcohol use. AST value is 2× ALT value (“ToAST 2 ALcohol”). Treatment: benzodiazepines.


First_Aid_Step1

First_Aid_Step1. Nonspecific: mood elevation, • appetite, Nonspecific: post-use “crash,” including psychomotor agitation, insomnia, cardiac depression, lethargy,  appetite, sleep arrhythmias, tachycardia, anxiety. disturbance, vivid nightmares. Alcohol use disorder Physiologic tolerance and dependence on alcohol with symptoms of withdrawal when intake is interrupted. Complications: vitamin B1 (thiamine) deficiency, alcoholic cirrhosis, hepatitis, pancreatitis, peripheral neuropathy, testicular atrophy. Treatment: naltrexone (reduces cravings), acamprosate, disulfiram (to condition the patient to abstain from alcohol use). Support groups such as Alcoholics Anonymous are helpful in sustaining abstinence and supporting patient and family.


First_Aid_Step1

First_Aid_Step1. Wernicke-Korsakoff Results from vitamin B1 deficiency. Symptoms can be precipitated by administering dextrose syndrome before vitamin B1. Triad of confusion, ophthalmoplegia, ataxia (Wernicke encephalopathy). May progress to irreversible memory loss, confabulation, personality change (Korsakoff syndrome). Treatment: IV vitamin B1 (before dextrose). Behavioral therapy Teaches patients how to identify and change maladaptive behaviors or reactions to stimuli. Examples include systematic desensitization for treatment of phobia. Cognitive behavioral Teaches patients to recognize distortions in their thought processes, develop constructive coping therapy skills, and • maladaptive coping behaviors • greater emotional control and tolerance of distress. Examples include recognizing triggers for alcohol consumption. Dialectical behavioral Designed for use in borderline personality disorder, but can be used in other psychiatric conditions therapy as well (eg, depression).


First_Aid_Step1

First_Aid_Step1. Dialectical behavioral Designed for use in borderline personality disorder, but can be used in other psychiatric conditions therapy as well (eg, depression). Interpersonal therapy Focused on improving interpersonal relationships and communication skills. Supportive therapy Utilizes empathy to help individuals during a time of hardship to maintain optimism or hope. for selected ADHD Stimulants (methylphenidate, amphetamines) psychiatric conditions Alcohol withdrawal Benzodiazepines (eg, chlordiazepoxide, lorazepam, diazepam) Generalized anxiety disorder SSRIs, SNRIs Obsessive-compulsive disorder SSRIs, venlafaxine, clomipramine Panic disorder SSRIs, venlafaxine, benzodiazepines PTSD SSRIs, venlafaxine MEchaNisM  catecholamines in the synaptic cleft, especially norepinephrine and dopamine. cliNical UsE ADHD, narcolepsy, binge-eating disorder. aDVErsE EFFEcts Nervousness, agitation, anxiety, insomnia, anorexia, tachycardia, hypertension, weight loss, tics, bruxism.


First_Aid_Step1

First_Aid_Step1. cliNical UsE ADHD, narcolepsy, binge-eating disorder. aDVErsE EFFEcts Nervousness, agitation, anxiety, insomnia, anorexia, tachycardia, hypertension, weight loss, tics, bruxism. Typical antipsychotics Haloperidol, pimozide, trifluoperazine, fluphenazine, thioridazine, chlorpromazine. MEchaNisM Block dopamine D2 receptor (• cAMP). cliNical UsE Schizophrenia (1° positive symptoms), psychosis, bipolar disorder, delirium, Tourette syndrome, Huntington disease, OCD. Use with caution in dementia. PotENcy High potency: Haloperidol, Trifluoperazine, Fluphenazine (Hal Tries to Fly High)—more neurologic side effects (eg, extrapyramidal symptoms [EPS]). Low potency: Chlorpromazine, Thioridazine (Cheating Thieves are low)—more anticholinergic, antihistamine, α1-blockade effects.


First_Aid_Step1

First_Aid_Step1. aDVErsE EFFEcts Lipid soluble  stored in body fat  slow to be removed from body. Endocrine: dopamine receptor antagonism • hyperprolactinemia  galactorrhea, oligomenorrhea, gynecomastia. Metabolic: dyslipidemia, weight gain, hyperglycemia. Antimuscarinic: dry mouth, constipation. Antihistamine: sedation. α1-blockade: orthostatic hypotension. Cardiac: QT prolongation. Ophthalmologic: Chlorpromazine—Corneal deposits; Thioridazine—reTinal deposits. Neuroleptic malignant syndrome. Extrapyramidal symptoms— ADAPT: Hours to days: Acute Dystonia (muscle spasm, stiffness, oculogyric crisis). Treatment: benztropine, diphenhydramine. Days to months: Akathisia (restlessness). Treatment: β-blockers, benztropine, benzodiazepines. Parkinsonism (bradykinesia). Treatment: benztropine, amantadine. Months to years: Tardive dyskinesia (chorea, especially orofacial). Treatment: atypical antipsychotics (eg, clozapine), valbenazine, deutetrabenazine.


First_Aid_Step1

First_Aid_Step1. Months to years: Tardive dyskinesia (chorea, especially orofacial). Treatment: atypical antipsychotics (eg, clozapine), valbenazine, deutetrabenazine. MAOIs AXON POSTSYNAPTIC NEURON Mirtazapine TCAs, SSRIs, SNRIs, trazodone MAO Metabolites ----NE NE reuptake ˜2 (autoreceptor) adrenergic receptor Metabolites 5-HT 5-HT reuptake 5-HT receptorNE receptor -MAO AXON -TCAs, SNRIs, bupropion Selective serotonin reuptake inhibitors Fluoxetine, fluvoxamine, paroxetine, sertraline, escitalopram, citalopram. MEchaNisM Inhibit 5-HT reuptake. It normally takes 4–8 weeks for antidepressants to show appreciable effect. cliNical UsE Depression, generalized anxiety disorder, panic disorder, OCD, bulimia, binge-eating disorder, social anxiety disorder, PTSD, premature ejaculation, premenstrual dysphoric disorder. aDVErsE EFFEcts Fewer than TCAs. Serotonin syndrome, GI distress, SIADH, sexual dysfunction (anorgasmia,  libido).


First_Aid_Step1

First_Aid_Step1. aDVErsE EFFEcts Fewer than TCAs. Serotonin syndrome, GI distress, SIADH, sexual dysfunction (anorgasmia,  libido). Serotoninnorepinephrine reuptake inhibitors Venlafaxine, desvenlafaxine, duloxetine, levomilnacipran, milnacipran. MEchaNisM Inhibit 5-HT and NE reuptake. cliNical UsE Depression, generalized anxiety disorder, diabetic neuropathy. Venlafaxine is also indicated for social anxiety disorder, panic disorder, PTSD, OCD. Duloxetine and milnacipran are also indicated for fibromyalgia. aDVErsE EFFEcts  BP, stimulant effects, sedation, nausea. Tricyclic Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine. antidepressants MEchaNisM TCAs inhibit 5-HT and NE reuptake. cliNical UsE MDD, peripheral neuropathy, chronic neuropathic pain, migraine prophylaxis, OCD (clomipramine), nocturnal enuresis (imipramine, although adverse effects may limit use).


First_Aid_Step1

First_Aid_Step1. cliNical UsE MDD, peripheral neuropathy, chronic neuropathic pain, migraine prophylaxis, OCD (clomipramine), nocturnal enuresis (imipramine, although adverse effects may limit use). aDVErsE EFFEcts Sedation, α1-blocking effects including postural hypotension, and atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). 3° TCAs (amitriptyline) have more anticholinergic effects than 2° TCAs (nortriptyline). Can prolong QT interval. Tri-CyCliC’s: Convulsions, Coma, Cardiotoxicity (arrhythmia due to Na+ channel inhibition); also respiratory depression, hyperpyrexia. Confusion and hallucinations are more common in the elderly due to anticholinergic side effects (2° amines [eg, nortriptyline] better tolerated). Treatment: NaHCO3 to prevent arrhythmia. Monoamine oxidase Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline (selective MAO-B inhibitor). inhibitors (MAO Takes Pride In Shanghai).


First_Aid_Step1

First_Aid_Step1. Monoamine oxidase Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline (selective MAO-B inhibitor). inhibitors (MAO Takes Pride In Shanghai). MEchaNisM Nonselective MAO inhibition  levels of amine neurotransmitters (norepinephrine, 5-HT, dopamine). cliNical UsE Atypical depression, anxiety. Parkinson disease (selegiline). aDVErsE EFFEcts CNS stimulation; hypertensive crisis, most notably with ingestion of tyramine. Contraindicated with SSRIs, TCAs, St. John’s wort, meperidine, dextromethorphan, linezolid (to avoid precipitating serotonin syndrome). Wait 2 weeks after stopping MAOIs before starting serotonergic drugs or stopping dietary restrictions. Bupropion Inhibits NE and DA reuptake. Also used for smoking cessation. Toxicity: stimulant effects (tachycardia, insomnia), headache, seizures in patients with bulimia and anorexia nervosa. Favorable sexual side effect profile.


First_Aid_Step1

First_Aid_Step1. Mirtazapine α2-antagonist ( release of NE and 5-HT), potent 5-HT2 and 5-HT3 receptor antagonist, and H1 antagonist. Toxicity: sedation (which may be desirable in depressed patients with insomnia), • appetite, weight gain (which may be desirable in underweight patients), dry mouth. Trazodone Primarily blocks 5-HT2, α1-adrenergic, and H1 receptors; also weakly inhibits 5-HT reuptake. Used primarily for insomnia, as high doses are needed for antidepressant effects. Toxicity: sedation, nausea, priapism, postural hypotension. Think traZZZobone due to sedative and male-specific side effects. Varenicline Nicotinic ACh receptor partial agonist. Used for smoking cessation. Toxicity: sleep disturbance, depressed mood, suicidal ideation. Varenicline helps nicotine cravings decline. Methadone Long-acting oral opiate used for heroin detoxification or long-term maintenance therapy. Buprenorphine Sublingual form (partial agonist) used to prevent relapse.


First_Aid_Step1

First_Aid_Step1. Methadone Long-acting oral opiate used for heroin detoxification or long-term maintenance therapy. Buprenorphine Sublingual form (partial agonist) used to prevent relapse. Naloxone Short-acting opioid antagonist given IM, IV, or as a nasal spray to treat acute opioid overdose, particularly to reverse respiratory and CNS depression. Naltrexone Long-acting oral opioid antagonist used after detoxification to prevent relapse. Use naltrexone for the long trex back to sobriety. “But I know all about love already. I know precious little still about kidneys.” —Aldous Huxley, Antic Hay “This too shall pass. Just like a kidney stone.” “I drink too much. The last time I gave a urine sample it had an olive in it.”


First_Aid_Step1

First_Aid_Step1. Being able to understand and apply renal physiology will be critical for the exam. Important topics include electrolyte disorders, acid-base derangements, glomerular disorders (including histopathology), acute and chronic kidney disease, urine casts, diuretics, ACE inhibitors, and AT-II receptor blockers. Renal anomalies associated with various congenital defects are also high-yield associations to think about when evaluating pediatric vignettes. Kidney embryology Pronephros—week 4; then degenerates. Mesonephros—functions as interim kidney for 1st trimester; later contributes to male genital system. Metanephros—permanent; first appears in 5th week of gestation; nephrogenesis continues through weeks 32–36 of gestation. Ureteric bud (metanephric diverticulum)— derived from caudal end of mesonephric duct; gives rise to ureter, pelvises, calyces, collecting ducts; fully canalized by 10th week


First_Aid_Step1

First_Aid_Step1. Ureteric bud (metanephric diverticulum)— derived from caudal end of mesonephric duct; gives rise to ureter, pelvises, calyces, collecting ducts; fully canalized by 10th week Metanephric mesenchyme (ie, metanephric blastema)—ureteric bud interacts with this tissue; interaction induces differentiation and formation of glomerulus through to distal convoluted tubule (DCT) Aberrant interaction between these 2 tissues may result in several congenital malformations of the kidney (eg, renal agenesis, multicystic dysplastic kidney) Ureteropelvic junction—last to canalize  congenital obstruction. Most common cause of prenatal hydronephrosis. Detected by prenatal ultrasound. Oligohydramnios  compression of developing fetus  limb deformities, facial anomalies (eg, low-set ears and retrognathia A , flattened nose), compression of chest and lack of amniotic fluid aspiration into fetal lungs  pulmonary hypoplasia (cause of death).


First_Aid_Step1

First_Aid_Step1. Causes include ARPKD, obstructive uropathy (eg, posterior urethral valves), bilateral renal agenesis, chronic placental insufficiency. Babies who can’t “Pee” in utero develop Potter sequence. POTTER sequence associated with: Pulmonary hypoplasia Oligohydramnios (trigger) Twisted face Twisted skin Extremity defects Renal failure (in utero) Inferior poles of both kidneys fuse abnormally A . As they ascend from pelvis during fetal development, horseshoe kidneys get trapped under inferior mesenteric artery and remain low in the abdomen. Kidneys function normally. Associated with hydronephrosis (eg, ureteropelvic junction obstruction), renal stones, infection,  risk of renal cancer. Higher incidence in chromosomal aneuploidy (eg, Turner syndrome, trisomies 13, 18, 21). *Components of glomerular fltration barrier. Cross-section of glomerulus Left kidney is taken during living donor transplantation because it has a longer renal vein. Afferent = Arriving. Efferent = Exiting.


First_Aid_Step1

First_Aid_Step1. Cross-section of glomerulus Left kidney is taken during living donor transplantation because it has a longer renal vein. Afferent = Arriving. Efferent = Exiting. Renal blood flow: renal artery  segmental artery • interlobar artery  arcuate artery A • efferent arteriole  vasa recta/peritubular capillaries • venous outflow. Left renal vein receives two additional veins: left suprarenal and left gonadal veins. Despite high overall renal blood flow, renal medulla receives significantly less blood flow than renal cortex  very sensitive to hypoxia  vulnerable to ischemic damage. Course of ureters Course of ureter A : arises from renal pelvis, Water (ureters) flows over the iliacs and under travels under gonadal arteries • over common the bridge (uterine artery or vas deferens). (retroperitoneal). Gynecologic procedures (eg, ligation of  ureteral obstruction or leak. (in female) Bladder contraction compresses the intravesical ureter, preventing urine reflux.