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USMLE 1 > Neurology- Neurophatology > Flashcards

Neurology- Neurophatology Flashcards

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USMLE® Step 1 flashcards
1
Q

Common brain lesions

  • Frontal lobe
  • Frontal eye fields
A

Disinhibition and deficits in concentration, orientation, judgment; primitive reflexes.

Eyes look toward (destructive) side of lesion. In seizures (irritative), eyes look away from side of the lesion.

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2
Q

Common brain lesions

  • Paramedian pontine reticular formation
  • Medial longitudinal fasciculus
A

Ipsilateral gaze palsy (inability to look toward side of lesion).

Internuclear ophthalmoplegia (impaired adduction of ipsilateral eye; nystagmus of contralateral eye with abduction).

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3
Q

Common brain lesions

  • Dominant parietal cortex
  • Nondominant parietal cortex
A

Agraphia, acalculia, finger agnosia, left-right disorientation (Gestmann Sx).

Agnosia of the contralateral side of the world. (Hemispatial neglect syndrome)

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4
Q

Common brain lesions

  • Hippocampus (bilateral)
  • Basal ganglia
  • Subthalamic nucleus
A

Anterograde amnesia

May result in tremor at rest, chorea, athetosis.

Contralateral hemiballismus

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5
Q

Common brain lesions

- Mammillary bodies (bilateral)

A

Wernicke-Korsakoff syndrome—Confusion, Ataxia, Nystagmus, Ophthalmoplegia, memory loss, confabulation, personality changes.

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6
Q

Common brain lesions

  • Amygdala (bilateral)
  • Dorsal midbrain
A

Klüver-Bucy syndrome—disinhibited behavior (HSV-1 encephalitis)

Parinaud syndrome—vertical gaze palsy, pupillary light-near dissociation, lid retraction, convergence-retraction nystagmus. (Stroke, hydrocephalus, pinealoma)

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7
Q

Common brain lesions

  • Reticular activating system (midbrain)
  • Cerebellar hemisphere
  • Cerebellar Vermis
A

Reduced levels of arousal and wakefulness (eg, coma).

Intention tremor, limb ataxia, loss of balance; ipsilateral deficits; fall toward side of lesion.

Truncal ataxia (wide-based, “drunken sailor” gait), dysarthria.

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8
Q

Common brain lesions

  • Decorticate (flexor) posturing
  • Decerebrate (extensor) posturing
A

lesion above red nucleus, presents with flexion of upper extremities and extension of lower extremities.

Lesion at or below red nucleus, presents with extension of upper and lower extremities.

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9
Q

Ischemic brain disease/stroke

  • Most vulnerable areas
  • Stroke imaging
A

hippocampus, neocortex, cerebellum (Purkinje cells), watershed areas.

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.

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10
Q

Ischemic stroke

  • Types
  • Treatment
A

Thrombotic, embolic, hypoxic

tPA (if within 3–4.5 hr). Medical therapy (eg, aspirin, clopidogrel); optimum control of blood pressure, blood sugars, lipids; and treat conditions that  risk (eg, atrial fibrillation, carotid artery stenosis).

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11
Q

Neonatal intraventricular hemorrhage

A

Bleeding into ventricles. 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.

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12
Q

Intracranial hemorrhage

- Epidural

A

Rupture of middle meningeal artery (pterion).

Scalp hematoma and rapid intracranial expansion under systemic arterial pressure Ž transtentorial
herniation, CN III palsy.

CT shows biconvex (lentiform), hyperdense blood collection

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13
Q

Intracranial hemorrhage

- Subdural

A

Rupture of bridging veins. Seen in shaken babies. Predisposing: brain atrophy, Trauma.

Crescent-shaped hemorrhage that crosses suture lines. Can cause midline shift, findings of “acute on chronic” hemorrhage.

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14
Q

Intracranial hemorrhage

- Subarachnoid hemorrhage

A

Bleeding due to trauma, or rupture of an aneurysm, or arteriovenous malformation. Patients complain of “worst headache of my life.”

Xanthochromic spinal tap. Vasospasm can occur due to
blood breakdown or rebleed 3–10 days after hemorrhage Ž ischemic infarct; nimodipine used to prevent/reduce vasospasm.

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15
Q

Intracranial hemorrhage

- Intraparenchymal hemorrhage

A

by systemic hypertension. Also seen with amyloid
angiopathy. 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), followed by thalamus, pons, and cerebellum.

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16
Q

Effects of strokes

A

Pag. 498, 499

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17
Q

Diffuse axonal injury

A

Caused by traumatic shearing forces during rapid acceleration and/or deceleration of the brain.

devastating neurologic injury, often causing coma or
persistent vegetative state

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18
Q

Lateral medullary (Wallenberg) syndrome

A

Nucleus ambiguus effects are specific to PICA lesions.

“Don’t pick a (PICA) horse (hoarseness) that can’t eat
(dysphagia).”

Also supplies inferior cerebellar peduncle (part of cerebellum).

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19
Q

Lateral pontine syndrome

A

Facial nucleus effects are specific to AICA lesions.

“Facial droop means AICA’s pooped.”

Also supplies middle and inferior cerebellar peduncles (part of cerebellum).

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20
Q

aphasias

A

higher-order language deficit (inability to understand/produce/use language appropriately)

Pag. 500

21
Q

Saccular aneurysm (berry)

A

Occurs at bifurcations in the circle of Willis. Most common site is junction of ACom and ACA. Associated with ADPKD, Ehlers-Danlos syndrome.

Usually clinically silent until rupture Ž subarachnoid hemorrhage Ž focal neurologic deficits

22
Q

Saccular aneurysm (berry)

  • ACom
  • MCA
  • PCom
A

Bitemporal hemianopia; ischemia in ACA distribution Ž contralateral lower extremity hemiparesis, sensory deficits.

Ischemia in MCA distribution Ž contralateral upper extremity and lower facial hemiparesis, sensory deficits.

Ipsilateral CN III palsy Ž mydriasis (“blown pupil”); may also see ptosis, “down and out” eye

23
Q

Partial (focal) seizures

  • Types
A

ƒƒ Simple partial (consciousness intact)—motor, sensory, autonomic, psychic

ƒƒ Complex partial (impaired consciousness,
automatisms)

24
Q

Generalized seizures

- Types

A

ƒƒ Absence (petit mal)—3 Hz spike-and-wave discharges, no postictal confusion, blank stare

ƒƒMyoclonic—quick, repetitive jerks

ƒƒ Tonic-clonic (grand mal)—alternating stiffening and movement

ƒƒ Tonic—stiffening

ƒƒ Atonic—“drop” seizures (falls to floor); commonly mistaken for fainting

25
Q

Epilepsy

Status epilepticus

A

disorder of recurrent seizures (febrile seizures are not epilepsy).

Continuous (≥ 5 min) or recurring seizures that may result in brain injury.

26
Q

Cluster Headaches

  • Localization and Duration
  • Description
  • Treatment
A

Unilateral. 15 min–3 hr; repetitive

Excruciating periorbital pain (“suicide headache”) with
lacrimation and rhinorrhea. May present with Horner
syndrome. More common in males.

Acute: sumatriptan, 100% O2
Prophylaxis: verapamil

27
Q

Tension Headaches

  • Localization and Duration
  • Description
  • Treatment
A

Bilateral. > 30 min (typically 4–6 hr); constant

Steady, “band-like” pain. No photophobia or phonophobia. No aura.

Analgesics, NSAIDs, acetaminophen; amitriptyline for chronic pain

28
Q

Migraine Headaches

  • Localization and Duration
  • Description
  • Treatment
A

Unilateral. 4–72 hr

POUND–Pulsatile, One-day duration, Unilateral, Nausea,Disabling

Acute: NSAIDs, triptans, dihydroergotamine
Prophylaxis: lifestyle changes, β-blockers, amitriptyline,
topiramate, valproate.

29
Q

Movement disorders

A

Pag. 503

30
Q

Parkinson

- Clinical manifestations

A 
Parkinson TRAPS your body:
Tremor (pill-rolling tremor at rest)
Rigidity (cogwheel)
Akinesia (or bradykinesia)
Postural instability
Shuffling gait
31
Q

Parkinson

- Etiology

A

MPTP, a contaminant in illegal drugs, is metabolized to MPP+, which is toxic to substantia nigra.

Loss of dopaminergic neurons of substantia nigra pars
compacta.
Lewy bodies: composed of α-synuclein.

32
Q

Huntington disease

  • Etiology
  • Clinical presentation
A

Caudate loses ACh and GABA. (CAG) repeat expansion in the huntingtin (HTT) gene on chromosome 4 (4 letters). AD

Between ages 20 and 50: chorea, athetosis, aggression, depression, dementia

33
Q

Alzheimer disease

- Proteins associated

A

APP is located on chromosome 21. Most common cause of dementia.

Associated with the following altered proteins:
ƒƒ ApoE-2: risk of sporadic form
ƒƒ ApoE-4: risk of sporadic form
ƒƒ APP, presenilin-1, presenilin-2: familial forms (10%) with earlier onset

34
Q

Alzheimer disease

- Histology and gross findings

A

Senile plaques in gray matter: extracellular β-amyloid core; may cause amyloid angiopathy Ž intracranial hemorrhage; Aβ (amyloid-β) synthesized by cleaving amyloid precursor protein (APP).

Neurofibrillary tangles: intracellular, hyperphosphorylated tau protein; number of tangles
correlates with degree of dementia

35
Q

Frontotemporal dementia (Pick disease)

  • Clinical presentation
  • Etiology
A

Early changes in personality and behavior (behavioral variant), or aphasia (primary progressive aphasia). May have associated movement disorders

Inclusions of hyperphosphorylated tau (round Pick bodies) or ubiquitinated TDP-43.

36
Q

Lewy body dementia

- Clinical presentation

A

Visual hallucinations, dementia with fluctuating cognition/ alertness, REM sleep behavior disorder, and
parkinsonism.

Called Lewy body dementia if cognitive and motor symptom onset < 1 year apart, otherwise considered dementia 2° to Parkinson disease.

37
Q

Vascular dementia

  • Epidemiology
  • Etiology
A

2nd most common cause of dementia

Result of multiple arterial infarcts and/or chronic ischemia.

38
Q

Creutzfeldt-Jakob disease

  • Clinical presentation
  • EEG and CSF marker
  • Etiology
A

Rapidly progressive dementia with myoclonus and ataxia.

Commonly see periodic sharp waves on EEG and  14-3-3 protein in CSF.

Spongiform cortex. Prions (PrPc Ž PrPsc sheet [β-pleated sheet resistant to proteases])

39
Q

Idiopathic intracranial hypertension (pseudotumor cerebri)

  • Risk factors
  • Clinical findings
  • Treatment
A

Risk factors include female gender, Tetracyclines, Obesity, vitamin A excess, Danazol (female TOAD).

Findings: headache, tinnitus, diplopia, no change in mental status. Papilledema. Lumbar puncture reveals increase opening pressure

Treatment: weight loss, acetazolamide, invasive procedures for refractory cases.

40
Q

Normal pressure hydrocephalus

A

Affects the elderly; idiopathic

Expansion of ventricles distorts the fibers of the corona radiata Ž Triad of urinary incontinence, gait apraxia (magnetic gait), and cognitive dysfunction.

41
Q

Ex vacuo ventriculomegaly

A

Appearance of increase CSF on imaging, but is actually due to decrease brain tissue and neuronal atrophy. ICP is normal; NPH triad is not seen.

42
Q

Multiple sclerosis

- Presentation

A

ƒƒ Acute optic neuritis (Marcus Gunn pupil)
ƒƒ Brain stem/cerebellar syndromes
ƒƒ Pyramidal tract weakness
ƒƒ Spinal cord syndromes (Lhermitte phenomenon, neurogenic bladder, paraparesis, sensory)

43
Q

Multiple sclerosis

- Findings

A

Increase IgG level and myelin basic protein in CSF.

Oligoclonal bands are diagnostic.

MRI is gold standard. Periventricular plaques. Multiple
white matter lesions disseminated in space and time.

44
Q

Osmotic demyelination syndrome (central pontine myelinolisis)

  • Etiology
  • Clinical presentation
A

Massive axonal demyelination in pontine white matter 2° to rapid osmotic changeS.

Acute paralysis, dysarthria, dysphagia, diplopia, loss of
consciousness. Can cause “locked-in syndrome.”

45
Q

Acute inflammatory demyelinating polyradiculopathy

  • Phatophysiology
  • Clinical presentation
A

Guillain-Barré syndrome. Autoimmune condition associated with infections that destroys Schwann cells.

Symmetric ascending muscle weakness/paralysis and depressed/absent DTRs. Facial paralysis and respiratory failure. May see autonomic dysregulation or sensory abnormalities.

*Increase CSF protein with normal cell count

46
Q

Acute disseminated (postinfectious) encephalomyelitis

  • Phatophysiology
  • Clinical presentation
A

Multifocal inflammation and demyelination after infection or vaccination.

Presents with rapidly progressive multifocal neurologic symptoms, altered mental status.

47
Q

Charcot-Marie-Tooth disease (hereditary motor and sensory neuropathy)

  • Phatophysiology
  • Clinical presentation
A

Defective production of proteins involved in the structure and function of peripheral nerves. Most common type, CMT1A, is caused by PMP22 gene duplication. AD

Associated with foot deformities, lower extremity weakness and sensory deficits.

48
Q

Progressive multifocal leukoencephalopathy

  • Phatophysiology
  • Clinical presentation
A

Demyelination of CNS due to destruction of oligodendrocytes (2° to reactivation of latent
JC virus infection).

Seen in 2–4% of patients with AIDS. Risk
associated with natalizumab, rituximab.

49
Q

Other demyelinating and dysmyelinating disorders

A

Krabbe disease, metachromatic leukodystrophy, adrenoleukodystrophy

USMLE 1 (73 decks)

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