Step Up - Neuro Flashcards

1
Q

Define TIA. What is the pathophysiology (2)? How does it resolve (2)? What is the risk of stroke following TIA? How is it treated?

A

1) TIA = neurologic deficit lasting less than 24 hours. Differentiated from stroke based on duration of symptoms
2) Pathophys: caused by emboli, or transietn hypotension due to carotid stenosis
3) Collateral reperfusion or break-up of emboli
4) 10% per year. 30% 5-yr risk of stroke
5) Tx: modify cardiac risk factors to prevent stroke

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2
Q

What are the major (2) and minor risk (9) factors for stroke?

A

1) HTN and age

2) smoking, DM, hyperlipidemia, Afib, CAD, Fam Hx, past TIA, carotid bruits, hypercoagulable states

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3
Q

What are four major causes of ischemic stroke?

A

1) Emboli - origin: heart, internal carotid, aorta, paradoxical (requires heart defect)
2) Thombotic - atheroscleotic plaques in large and medium sized vessels
3) Lacunar stroke - small vessel thrombotic disease
4) Nonvacular causes - low CO, anoxia

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4
Q

Briefly describe the deficits seen in the following ischemic strokes: anterior cerebral artery, middle cerebral artery, vetebral/basilar, Lacunar (internal capsule, pons, thalamus)

A

1) Anterior - contralateral lower extremity and face
2) Middle - aphasia, contralateral hemiparesis
3) Vertebral/Basilar - ataxia, diplopia, dysphagia, dysarthria, vertigo, hemianopsia
4) Lacunar - IC: pure motor hemiparesis
5) Lacunar - Pons: dysarthria, clumsy hand
6) Lacunar - Thalamus: Pure sensory deficit

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5
Q

How are ischemic strokes treated (4)?

A

1) Supportive - airway, oxygen, IV fluids
2) tPA - if within 3 hours (contraindicated if: uncontrolled HTN, bleeding disorder, anticoagulants, recent surgery)
3) Aspirin or clopidogrel - if >3 hours
4) BP control if >220/120 or if receiving tPA

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6
Q

How are ischemic strokes prevented (3)?

A

1) Artherosclerosis
a) control RF: HTN, DM, smoking, high lipids
b) ASA
c) Surgery - carotid endarterectomy if >70% occluded and symptomatic.
2) Embolic - ASA
3) Lacunar - HTN control

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7
Q

What are the causes and complications of an intracerebral hemorrhage ()? What area of the brain is most commonly affected?

A

1) Caused by rapid elevation of BP
2) Complications: high ICP, seizure, vasospasm, hydrocephalus, SIADH
3) Basal ganglia

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8
Q

How is intracerebral hemorrhage treated (3)?

A

1) ICU and ABCs
2) BP control if >160/105, nitroprusside
3) Mannitol to reduce ICP if elevated

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9
Q

What are the clinical features of a subarchanoid hemorrhage (5)?

A

1) sudden and severe headache
2) LOC
3) vomiting
4) Meningismus - nuchal rigidity, photphobia
5) retinal hemorrhage

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10
Q

How is subarachnoid hemorrhage diagnosed (3)?

A

1) Noncontrast CT
2) Perform LP (confirm no elevated ICP fisrt)
- xanthochromia is diagnostic (lysed RBCs)
3) CTA

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11
Q

How is SAH treated (7)?

A

1) Surgical - clipping of aneurysms
2) Medical
a) rest in dark room
b) stool softeners to prevent straining (ICP)
c) Analgesia for headache
d) IV fluids
e) Control BP
f) CCB (nifedipine) to counter vasospasm

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12
Q

Describe the pathophysiology of parkinsons disease. What are the clinical features (9)?

A

1) loss of dopaminergic drive in basal ganglia (substantia nigra), leading to cholinergic dominance
2) Features: pill-rolling tremor at rest, bradykinesia, cogwheel rigidity, stooped posture, expressionless facies, dyarthria and dysgraphia, dementia, autonomic dysfunction (orthostatic hypotension), personality changes

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13
Q

What is the treatment for parkinson’s (5)?

A

1) Carbidopa-levodopa: increase dopamine drive
2) Dopamine-receptor agonists (bromocriptine)
3) MAO inhibitors (Selegiline): adjunct to increase dopamine action
4) Anticholinergic drugs
5) Amitriptyline - useful as anticholinergic and as antidepressant

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14
Q

Describe the clinical features of Huntington Chorea (5). How is it diagnosed (2)? How is it treated (2)?

A

1) features: chorea, altered behaviour, dementia, unsteady gait, incontinence
2) Dx: MRI of caudate nuclei, DNA tests (AD)
3) Tx: symptomatic - dopamine blockers, antidepressants

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15
Q

When is an essential tremor elicited? What improves it (2)? How is it treated?

A

1) Tremor with certain action (ex. drinking)
2) Not there with rest, improved with alcohol
3) Tx: propranolol

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16
Q

Describe tourettes syndrome (4). How is it treated (3)?

A

1) Features: associated with OCD, onset before 21, AD inheritance, must have motor and phonic tics
2) Tx: clonidine, pimozide, haloperidol

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17
Q

Provide the differential diagnoses for dementia organized under the headings: neurologic, infections, metabolic, drugs/toxins, and psychiatric (min 10).

A

1) Neuro - alzheimer’s, vascular dementia, space-oocupying lesions, lewy body, FT dementia
2) Infection- HIV, neurosyphilis, C-J disease
3) Metabolic - thyroid disease, vit b12 def., thiamine def., niacin def.
4) Drugs/toxins - alcoholism, heavy metals
5) Psych - depression

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18
Q

What is the triad of normal pressure hydrocephalus?

A
  • Wet, wacky, wobbly

- urinary incontinence, dementia, gait disturbances

19
Q

Describe the pahtology underlying alzheimer’s disease (2).

A

1) Senile plaques - focal, tortuous neuritic processes surronding a central amyloid core
2) Neurofibrillary tangles - neurofilaments in cytoplasm of neurons

20
Q

How is alzheimer’s diagnosed (2)? How is it treated (2)?

A

1) Dx: clinical, MRI shows atrophy with enlarged ventricles

2) Tx: AChE inhibitors as brain is deficient in ACh (donepezil). Possible benefit to high dose Vit. E.

21
Q

Provide the differential diagnosis for delirium using the pneumonic P. DIMM WIT (also see SMASHED for coma)

A
P - post operative
D - dehydration and malnutrition
I - Infection (UTI, meningitis, encephalitis)
M - medications and drugs (TCAs, corticosteroids, anticholinergics)
M - metals
W - withdrawal (alcohol, benzos)
I - Inflammation, fever
T - trauma, burns
22
Q

Provide the differential diagnosis for coma (and dementia) using the pneumonic SMASHED.

A
S - structural brain pathology (stroke, hematoma)
M - meningitis, mental illness
A - alcohol, acidosis
S - seizures
H - hyper/hypo - glc, temp, electrolytes
E - endocrine (Addison's)
D - drugs (opiates, benzos, CO
23
Q

Provide the glasgow coma scale

A

Eyes (4): open spontaneously, open to voice, open to pain, no response
Verbal (5): oriented, confused speech, inappropriate words, sounds, none
Motor (6): follows commands, localizes pain, flexion to pain, decorticate, deceribrate, none

24
Q

Discuss the diagnosis of MS. Describe the three categories of diagnosis - clinically definite MS, laboratory-supported definite MS, probable MS

A

1) Clinically definite MS - two episodes of symptoms, evidence of 2 white matter lesions
2) Laboratory-supported - two episodes of symptoms, evidence of at least one white matter lesion on MRI, abnormal CSF (oligoclonal bands)
3) Probable MS - two episodes of symptoms with either one white matter lesion or oligoclonal bands on CSF.

25
Q

What are the two visual disturbances associated with MS?

A

1) Optic neuritis - monocular visual loss

2) Internuclear ophthalmoplegia - medial rectus palsy (MLF lesion)

26
Q

How is MS diagnosed (4)?

A

1) Largely clinical Dx
2) MRI for lesions
3) LP - oligoclonal bands
4) Decreased nerve conduction on evoked potential study of brain

27
Q

How is MS treated (2)?

A

1) Acute attack - IV steroids

2) Disease modifying agents - interferon, cyclophosphamide

28
Q

Describe the pathophysiology, course, clinical features, diagnosis, and treatment of Guillain-Barre Syndrome

A

1) Patho - inflammatory demyelinating polyneuropathy affecting motor nerves
2) Course - preceded by illness
3) Features - rapid ascending weakness/paralysis, risk of resp arrest, sensation preserved.
4) Dx - CSF (protein high, cell count normal), decreased nerve conduction
5) Tx - support airway, IVIG, plasmapheresis if severe

29
Q

Describe the pathophysiology, course, clinical features, diagnosis, and treatment of Myasthenia Gravis

A

1) Patho - autoimmune disorder against neuromuscular jxn.
2) Course - N/A
3) Features - occular involvement (ptosis, diplopia), generalized weakness. Concern is resp involvement.
4) Dx - ACh receptor antibody test, EMG, improvement with AChE inhibitor meds
5) Tx - AChE inhibitor (pyridostigmine), thymectomy, immune suppression (steroids, azathioprine), plasmapheresis if severe

30
Q

Describe the pathophysiology, course, clinical features, diagnosis, and treatment of Duchene Muscular Dystrophy

A

1) Patho - x-linked recessive
2) Course - resp failure, death in 3rd decade
3) Features - Growers maneuver, proximal muscle involvement, pseudohypertrophy of calves
4) Dx - Serum CK hign, DNA testing (or muscle biopsy)
5) Tx - prednisone, surgery for scoliosis

31
Q

Describe the pathophysiology, course, clinical features, diagnosis, and treatment of Neurofibromatosis

A

1) Patho - AD
2) Course - N/A
3) Features - cafe au lait spots, neurofibromas, acoustic neuromas (many others)
4) Dx - N/A
5) Tx - surgery for complications

32
Q

Describe the pathophysiology, course, clinical features, diagnosis, and treatment of Syringomyelia

A

1) Patho - Arnolad-Chiari malformation typ.
2) Course - N/A
3) Features - typically asymptomatic, if symptomatic it includes loss of P/T on over shoulders
4) Dx - MRI (incidentiloma)
5) Tx - refer to neurosurg

33
Q

Describe the pathophysiology, course, clinical features, diagnosis, and treatment of Brown-Sequard

A

1) Patho - N/A
2) Course - hemisection of spinal cord
3) Features - contralateral loss of P/T, ipsilateral loss of V/T and motor fxn
4) Dx - MRI
5) Tx - prognosis good

34
Q

Describe the pathophysiology, course, clinical features, diagnosis, and treatment of Horner Syndrome

A

1) Patho - interuption of cervical spinal nerves
2) Course - N/A
3) Features - ipsilateral ptosis, miosis, anhidrosis
4) Dx - cause: idiopathic, pancoast tumor, internal carotid dissection, brainstem stroke, neck trauma
5) Tx - treat cause

35
Q

What are the two broad categories of vertigo? How are they differentiated?

A

1) Central vertigo - other neurologic findings present, generally cardiovascular risk factors present, nystagmus is bidirectional or vertical
2) Peripheral vertigo - lesions are cochlear or retrocochlear, onset is abrupt, accompanied by N/V, position plays large role. Brainstem deficits are absent except for tinnitus and hearing loss

36
Q

What are the types of peripheral vertigo (5)? Briefly describe each.

A

1) BPV - positional, benign. Treat with meclizine, resolves in 6 mo.
2) Meniere disease - vertigo/tinnitus/hearing loss, treat with Na restriction and diuretics
3) Acute labyrinthitis - viral infection of inner ear
4) Ototoxic drugs - aminoglycosides, loop diuretics
5) Acoustic neuroma - ataxia, unsteady gait, nystagmus, hearing loss, tinnitus

37
Q

What are the main causes of syncope (6)? Briefly describe each one.

A

1) Seizure disorder
2) Cardiac - Arrythmias, obstruction of flow, MI
3) Vasovagal syncope - most common, tilt-table test for Dx. Paradoxical withdrawal of sympathetic support of BP
4) Orthostatic hypotension - defect in vasomotor reflex, similar to vasovagal.
5) Cerebrovascular disease - rare, TIA of veterbrobasilar circulation
6) Other - metabolic, mechanical, medications
- Do EKG first in work-up, rule out cardiac causes

38
Q

Provide the causes of provoked seizures (hint: 4M’s, 4I’s).

A

1) Metabolic and electrolyte disturbance
2) Mass lesion
3) Missing drugs - anticonvulsants, EtOH
4) Misc - pseudoseizure, eclampsia, hypertensive encephalopathy
5) Intoxications - cocaine, Li, CO
6) Infection - sepsis
7) Ischemia - stroke, TIA
8) Increased ICP - trauma

39
Q

Classify epileptic seizure, provide a brief description of each (). What is the appropriate treatment?

A

1) Partial - Simple (maintains consciousness) or complex (consciousness impaired)
- tx: carbamazepine or phenytoin
2) Generalized - Tonic-Clonic (loss of consciousness) or absence (consciousness impaired, automatisms, pediatric population)
- T-C tx: carbamazepine and phenytoin
- Abs tx: ethosuximibe and valproic acid

40
Q

Describe ALS. What are the clinical features (3). How is it diagnosed? How is it treated?

A

1) Anterior horn and corticospinal tracts affected, purely motor disease
2) Features: upper and lower motor neuron signs, progressive muscle weakness. Maintenance of continence, cognitive function, sexual function throughout. Death from resp arrest.
3) Dx: clinical evidence, involvement of many areas of body.
4) Tx: none. glutamate-blocking agents may help.

41
Q

Define aphasia. What are the causes (4)? Briefly describe the 4 types.

A

1) Def: defect of language, lesion in dominant hemisphere
2) Causes: stroke, trauma, tumor, alzheimers
3) Types:
a) Wernicke (receptive) - impaired comprehension, word-salad
b) Broca (expressive) - impaired fluency, comprehension fine
c) Conduction - distrubance in repitition, involves communication between W and B areas.
d) Global - disturbance in all language function
- Tx: most recover spontaneously in first month.

42
Q

What is Bell’s palsy? What is the cause? How is it diagnosed and treated (3)?

A

1) hemifacial paralysis of muscles innervated by CN VII
2) Cause: unknown. Possible viral involvement HSV.
3) Dx: clinical
4) Tx: typically resolves. Can use steroids, acyclovir, surgical decompression

43
Q

What is trigemnial neuralgia (Tic Douloureux)? What are some features (2)? How is it diagnosed? How is it treated?

A

1) idiopathic involvement of of CN V2, V3. Very painful
2) features: brief and frequent attacks (ophthalmic branch spared). No motor or sensory paralysis.
3) Dx: clinical
4) Tx: carbamazepine, phenytoin. Relapsing/remitting course.