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Neurology Review Flashcards

Neurology – Comprehensive Review Notes (Video Transcript)

  • Overview of session and structure
    • Topics: neurology, orthopedics, rheumatology with emphasis on pearls and practical review for primary care.
    • Blueprint reference: PANRY and PANTS for neurology (simplified, not a deep dive into every topic).
    • Strategy: focus on common conditions, with slower pace for larger topics; let neurology wash over for minor topics; emphasize pearls, real-world relevance, and practical management.

Headache disorders

  • Migraine headache
    • Prevalence: affects roughly 10\% \text{ to } 15\% of population across ages and demographics.
    • Diagnosis: based on history and physical exam; clinical pearls are usually sufficient.
    • Core features: unilateral, fairly severe to debilitating headache lasting several hours; associated with nausea/vomiting and photophobia/phonophobia (light and sound sensitivity).
    • Prodrome: about 75\% of patients have a prodrome 2 days to 1 day before onset (e.g., food craving).
    • Aura: about 25\% have true aura 2 hours to 1 day prior (neurological phenomena).
    • Imaging indications: image with non-contrast head CT if this is the first headache of life, the worst headache of life, or if there are pattern changes, increasing frequency, location change, or abnormal exam.
    • Acute treatment (abortive): first line 0$ acetaminophen and 0$ ibuprofen; triptans as second-line (used only on days with migraine, not daily); avoid opioids due to rebound headache and misuse risk.
    • Prophylaxis (preventive): indicated for significant frequency/disability, overuse of acute meds, or failure of first/second-line abortive therapy.
    • Mainstays: antihypertensives (beta blockers like propranolol; calcium channel blockers).
    • Antidepressants (non-SSRI): amitriptyline, nortriptyline (for comorbidity with depression; avoid SSRIs in this context).
    • Anticonvulsants for comorbid conditions (e.g., seizure disorders).
    • CGRP antagonists: injectable and highly effective, but beyond the scope of PANS/primary care in this session.
  • Cluster headache
    • Demographics: tends to affect males more often.
    • Presentation: severe, unilateral headaches in short bursts with a pattern (circadian/seasonal pattern like first day of spring in the morning).
    • Duration and features: attacks last 15\text{ minutes to a few hours}; unilateral with autonomic symptoms on the same side (vasomotor signs: red eye, tearing, rhinorrhea).
    • Imaging: CT imaging is only needed if first/worst or pattern change; otherwise not routinely.
    • Abortive therapy: 100% oxygen via non-rebreather; second-line options include intranasal or injectable triptans.
    • Prevention: can be prevented with calcium channel blockers.
  • Tension-type headache
    • Features: mild-to-moderate pain; often bilateral (band-like);
    • Associated symptoms: can include nausea but typically less disabling than migraine.
    • Management: OTC analgesics (acetaminophen/ibuprofen), stress reduction, massage, hot bath.
  • Idiopathic intracranial hypertension (pseudotumor cerebri)
    • Presentation: headaches with papilledema on fundoscopy (increased intracranial pressure).
    • Imaging: non-contrast CT to rule out bleed or mass; LP confirms high opening pressure.
    • Management: acetazolamide to decrease CSF pressure; lifestyle modification and weight loss.

Head injuries and traumatic brain injury (TBI)

  • Glasgow Coma Scale (GCS)
    • Maximum score: GCS_{max}=15.
    • Components: eye, verbal, and motor responses; lower scores indicate reduced consciousness.
    • Terminology: coma, stupor, lethargy, obtunded are imprecise terms indicating different levels of consciousness; avoid over-reliance on these terms.
  • Epidemiology of head injury
    • Common in adolescents/young adults (risky behavior) and elderly (falls).
    • Severity categories based on GCS:
    • Mild head injury: GCS 13–15 (often concussion).
    • Moderate head injury: GCS < 13.
    • Severe head injury: GCS < 8 (intubate if this occurs).
  • Imaging and initial management
    • Non-contrast CT is the image of choice for head injury.
    • Mild head injuries: many can be managed at home after observation; rest is advised for ~7 days; avoid secondary injury (secondary impact syndrome).
    • Post-concussive syndrome: symptoms may persist >30 days; management is largely supportive.
  • Severe head injuries and hematomas
    • Subdural hematoma: crescent-shaped bleed between dura and brain (follows brain contour).
    • Epidural hematoma: lens-shaped (lentiform) bleed between skull and dura; may have a lucid interval followed by deterioration.
    • Both require coagulation studies and neurosurgical evaluation for potential evacuation.
  • Seizures and epilepsy (definitions and acute management)
    • Seizure vs epilepsy: epilepsy = unprovoked seizures; not all seizures imply epilepsy.
    • Status epilepticus: seizures lasting \ge 5\text{ minutes} or ongoing convulsions with no return to consciousness.
    • First seizure evaluation: non-contrast CT head, MRI later if needed, EEG, labs including electrolytes and glucose.
    • Acute management of status epilepticus (first-line): benzodiazepines (weight-based dosing; examples include lorazepam, diazepam, midazolam); second-line antiseizure meds (e.g., phenytoin, levetiracetam); search for underlying cause (e.g., hypoglycemia).
  • Ischemic stroke and TIAs
    • Incidence: ~800,000+ strokes per year in the US.
    • TIAs: transient neurologic deficits (<24 hours); same underlying pathophysiology as ischemic stroke but blood flow resumes.
    • Acute management: non-contrast head CT initially; assess NIH Stroke Scale; swallow study; carotid ultrasound; ECG and telemetry; labs (CBC, CMP, coagulation);
    • Secondary prevention: dual antiplatelet therapy (aspirin + clopidogrel) after TIA/stroke depending on risk; for cardioembolic strokes, anticoagulation (warfarin or DOACs such as rivaroxaban, apixaban).
    • Thrombolysis: alteplase (tPA) within 4.5\ \text{hours} of onset; eligibility depends on onset time and contraindications.
    • Carotid revascularization: carotid endarterectomy considered with 70\% - 99\% stenosis on the affected side, typically within ~2 weeks of the event; avoid endarterectomy in 100\% occlusion.
    • Hemorrhagic stroke considerations: higher mortality; imaging (non-contrast CT) shows bleed; management often requires neurosurgical intervention.
    • Hemorrhagic etiologies: intracerebral hemorrhage (often with markedly elevated blood pressure) and subarachnoid hemorrhage (SAH) often due to aneurysm or AV malformations; SAH presents with thunderclap headache and neck stiffness; acute imaging with non-contrast CT; if CT negative, lumbar puncture for xanthochromia.
    • Aneurysm screening: if first-degree relatives have aneurysms (or multiple relatives), consider MR angiography or CT angiography.
    • Subarachnoid hemorrhage management: urgent neurosurgical consultation; aneurysm clipping or endovascular securing as appropriate.
    • Classic MCA stroke clues (example): aphasia, gaze deviation toward the lesion, hemineglect or hemianopia depending on dominance; language and visual changes help localize to anterior circulation.
  • Stroke assessment workflow (summary)
    • Initial: history to determine onset and last seen normal; non-contrast CT head; EKG; labs; NG/feeding/swallow evaluation; carotid ultrasound; NIHSS scoring.
    • If ischemic stroke identified: consider tPA within the time window; evaluate contraindications; plan for long-term antithrombotic and risk-factor management.
  • Practical clinical pearls
    • Time-zero is often “last normal” time; remember clock-based treatment windows.
    • Check for contraindications to tPA (recent surgery, bleeding disorders, severe hypertension, etc.).
    • In suspected TIA or minor stroke with improving symptoms, monitor and further investigate rather than immediately proceeding with thrombolysis.

Brain neoplasms

  • Presentation and imaging
    • Neurological symptoms such as new headaches or new-onset seizures prompt MRI brain with contrast.
  • Common primary brain tumors
    • Meningiomas, glioblastomas, pituitary adenomas.
  • Common metastatic patterns
    • Cancers with brain metastases: lung, melanoma, kidney, breast cancers.
  • Treatment approach
    • Management depends on symptoms and tumor type; MRI findings guide therapy choices.

Movement disorders

  • Essential tremor
    • Also called primary or familial tremor; action or postural tremor that improves with rest.
    • Alcohol can transiently reduce tremor in many cases.
    • Treatment: propranolol; also occupational therapy; caution in elderly or those with hypotension.
  • Parkinson's disease
    • Neurodegenerative with dopamine deficiency and acetylcholine excess; four cardinal signs:
    • Tremor at rest
    • Rigidity
    • Akinesia/bradykinesia
    • Postural instability
    • Other signs: shuffling gait, cogwheel rigidity, masked facies, hypophonia.
    • Treatment: primarily dopaminergic therapy – carbidopa-levodopa (carbidopa enhances brain access of levodopa) and dopamine agonists (pramipexole, ropinirole, bromocriptine).
  • Restless leg syndrome
    • Urge to move legs; occurs while awake; often with iron deficiency (check ferritin).
    • Treatments: gabapentinoids (pregabalin, gabapentin); dopamine agonists (roprinirole, pramipexole); sometimes carbidopa-levodopa.
  • Huntington's disease
    • Autosomal dominant on chromosome 4 with anticipation; choreiform movements; depression, dementia; typically onset in 30s–40s.
    • No cure; treatment is supportive; agents like tetrabenazine, deutetrabenazine, and valbenazine can help chorea; genetic counseling recommended.
  • Tardive dyskinesia (TD)
    • Extrapyramidal symptom often due to antipsychotics or metoclopramide; orofacial movements, tongue thrusting, lip smacking, or repetitive movements; may occur after short or long-term use.
    • Management: discontinue offending agent or switch to a second-generation antipsychotic; tetrabenazine or valbenazine may help; emphasize informed consent when prescribing medications with risk of TD.
  • Tourette syndrome
    • Motor and vocal tics with high comorbidity (OCD, ADHD, learning disorders).
    • Treatment: emphasize therapy (CBT) and management of comorbidities; medications for comorbids (e.g., SSRIs for anxiety) as appropriate.

Neurocognitive disorders

  • Dementia overview

    • Primary presentation: cognitive decline with memory impairment plus executive dysfunction; two main themes: memory loss and executive dysfunction.
    • Workup for cognitive decline includes ruling out reversible causes:
    • Thyroid disease, B12 deficiency, Lyme disease, tertiary syphilis.
    • Screening tools: Mini-Mental State Exam (MMSE), Montreal Cognitive Assessment (MoCA), Mini-Cog, etc.
    • Diagnostic imaging: MRI brain used to characterize structural changes.

  • Alzheimer’s disease

    • Major risk factor: age; risk increases with age (doubles every 5 years after 65).
    • Pathophysiology: amyloid beta plaques and tau tangles; APOE genotype influences risk.
    • Diagnosis: historically biopsy was gold standard but not performed in practice; diagnosis is clinical with supportive imaging and biomarkers.
    • Treatment: central cholinesterase inhibitors (donepezil, rivastigmine, galantamine) and NMDA receptor antagonist memantine; disease-modifying amyloid-targeting therapies are emerging but not routine in primary care.

  • Vascular dementia

    • Due to cumulative vascular insults (strokes/TIAs) with stepwise decline; imaging shows prior ischemic changes.
    • Management focuses on vascular risk factor control and prevention of further events; cholinesterase inhibitors have mixed evidence.

  • Lewy body dementia

    • Overlaps with Parkinson’s disease pathology (alpha-synuclein); fluctuating cognition with prominent visuospatial deficits; parkinsonian features.

  • Frontotemporal dementia

    • Early onset; prominent behavioral and personality changes (disinhibition) rather than memory loss.

  • Normal pressure hydrocephalus (NPH)

    • Triad: cognitive decline, urinary incontinence, magnetic/apraxic gait; ventriculomegaly out of proportion to cortical atrophy.
    • Management: high-volume lumbar puncture to remove CSF; if improvement, consider shunt placement.

  • Delirium and encephalopathy (conceptual overview)

    • Encephalopathy = broad term for brain dysfunction; delirium is often the acute, fluctuating disturbance in attention and cognition.
    • Common reversible causes: medications/toxins, electrolyte disturbances (e.g., hyponatremia, hypomagnesemia), infections, metabolic derangements (e.g., DKA), hypoglycemia, systemic illness.
    • Prevention and management: identify reversible cause, maintain orientation, preserve day-night cycles, ensure glasses/hearing aids, avoid benzodiazepines and anticholinergics when possible.
    • Delirium increases mortality and risk of long-term cognitive impairment.

Demyelinating and autoimmune CNS disorders

  • Multiple sclerosis (MS)
    • Central demyelination of CNS (brain/spinal cord).
    • Typical presentation: relapsing-remitting with transient focal neurologic symptoms (weakness, paresthesias, optic neuritis).
    • Diagnosis: MRI with contrast showing white matter lesions; Dawson's fingers (periventricular plaques aligned with venous structures).
    • CSF findings: oligoclonal bands.
    • Acute relapse treatment: high-dose steroids (e.g., prednisone) with taper.
    • Disease-modifying therapies: injectable agents like interferon beta and glatiramer acetate; newer monoclonal antibodies exist but are beyond this talk.

Neuromuscular and peripheral disorders

  • Myasthenia gravis (MG)
    • Autoimmune disease: antibodies block acetylcholine at the neuromuscular junction.
    • Clinical feature: fatigable weakness, often bulbar (face/neck/respiratory muscles); diaphragmatic weakness can cause respiratory failure (myasthenic crisis).
    • Diagnosis: acetylcholine receptor antibodies; thymus often harboring thymoma; chest CT to look for thymoma.
    • Treatment: acetylcholine esterase inhibitors (pyridostigmine) for symptom control; immunosuppression (steroids, cyclosporine, tacrolimus); rapid immunomodulation (plasmapheresis or IVIG) during crisis; thymectomy for thymoma.
  • Muscular dystrophy (e.g., Duchenne)
    • X-linked inheritance; early proximal weakness in children; elevated CPK; progressive wheelchair dependence in early adolescence.
  • Cerebral palsy
    • Non-progressive central motor dysfunction from birth or early infancy; variegated etiologies (anoxic injury, perinatal brain injury).
    • Key features: spasticity, contractures; management is supportive (PT/OT, speech therapy); orthotics and sometimes surgical realignment.
  • Amyotrophic lateral sclerosis (ALS)
    • Upper motor neuron signs (cerebral cortex) + lower motor neuron signs (anterior horn cells).
    • Symptom pattern: mixed paresis, spasticity, hyperreflexia; bulbar involvement (dysphagia, dysarthria, dyspnea).
    • No cure; referral for specialty care and multidisciplinary management.
  • Botulism
    • Clostridium botulinum infection; causes neuromuscular blockade similar to MG.
    • Key sources: raw honey in children <12 years due to immature antibodies; home canned foods, wild animals.
    • Diagnosis: lab confirmation; public health reporting.
    • Treatment: supportive; antitoxin; early recognition is critical.
  • Complex regional pain syndrome (CRPS)
    • Following minor trauma with disproportionate pain, redness/edema or temperature changes; dystrophic changes can be seen on imaging.
    • Management: NSAIDs, physical/occupational therapy; focus on functional recovery and pain control.
  • Guillain–Barré syndrome (GBS)
    • Autoimmune peripheral demyelination; often precipitated by infection, immunization, or surgery.
    • Presentation: ascending paralysis (distal to proximal); potential respiratory failure requiring ICU care.
    • Treatment: IVIG or plasmapheresis; most patients recover with time.
    • Important: GBS is a peripheral nervous system disorder (not MS, which is central).
  • Peripheral neuropathy
    • Common etiologies include diabetes mellitus (diabetic neuropathy).
    • Pattern: stocking-glove distribution (distal paresthesias, numbness, tingling); loss of proprioception.
    • Screening: monofilament testing (often the 10-gram filament) on feet and hands; emphasis on foot care.
    • Management: neuropathic pain medications (gabapentinoids such as gabapentin and pregabalin; duloxetine as an SNRI).
  • Cranial nerves (overview and practical mnemonic tips)
    • Remember order and function of cranial nerves; memorize sensory/motor/autonomic distinctions.
    • Practical tip: CN VII (facial nerve) vs CN III (oculomotor) differences can be remembered via eyelid movement:
    • CN VII controls eyelid closure; CN III controls eyelid opening; use a “pillar” analogy for eyelid positioning.
  • Bell’s palsy
    • Unilateral facial nerve (CN VII) palsy with inability to close the eye and drooping; dry nose/mouth due to impaired lacrimation and salivation.
    • Common precipitant: herpes simplex zoster/herpes infection.
    • Management: prednisone in high dose for 5–7 days if started within 3 days of onset; antivirals debated; eye lubrication/patching to prevent corneal injury.

Orthopedics-related neurology topics (brief intro bridging to ortho/rheumatology)

  • Carpal tunnel syndrome
    • Median nerve compression; distribution includes the thumb, index finger, middle finger, and radial half of the ring finger; palm involvement.
    • Diagnostic tests: Tinel’s sign, Phalen’s maneuver; clinical diagnosis often sufficient.
    • Management: nighttime splinting for severe cases; EMG/nerve conduction studies to confirm; surgical decompression if needed.
  • Spinal cord and radiculopathy basics
    • Nerve roots arising from the spinal cord; radiculopathy results from compression by herniated disc, arthritis, tumor, or infection.
    • Dermatomal maps to localize nerve involvement (examples):
    • L4: anterior thigh and knee; sensory and motor signs include quadriceps extension and patellar reflex.
    • L5: top of foot.
    • S1: bottom of foot; reflex Achilles.
    • C6: biceps and brachioradialis reflex; C7: triceps; C8: forearm/pinky finger.
    • Cauda equina syndrome: emergent surgical condition with triad of urinary retention, fecal incontinence, and saddle anesthesia; requires stat MRI and decompression.
    • Epidural abscess: red flags with long-standing back pain requiring imaging.

Key practical/ethical notes and takeaways

  • Imaging and interventions in acute neurology require balancing urgency with safety; use non-contrast CT as first-line imaging in head trauma, stroke, and suspected intracranial hemorrhage.
  • Thrombolysis (tPA) window is time-sensitive: 4.5\ \text{hours} from onset or last normal for eligible patients; contraindications should be carefully screened.
  • For MG and similar neuromuscular disorders, anticipate respiratory compromise; thymus pathology (thymoma) has important diagnostic and therapeutic implications.
  • In movement disorders, polypharmacy and comorbid conditions are common; tailor therapy to individual risk factors (e.g., hypotension with β-blockers in elderly patients).
  • In neurocognitive disorders, differentiate Alzheimer’s disease, vascular dementia, Lewy body dementia, and frontotemporal dementia; use appropriate imaging and targeted therapies; address reversible contributors first (thyroid, B12, infectious etiologies).
  • Delirium prevention focuses on maintaining orientation and sensory input, minimizing deliriogenic medications, and addressing reversible causes; preventable factors markedly influence mortality and functional outcomes.
  • Complex interplay between neurology and psychiatry: conditions like Huntington’s disease, Tourette syndrome, and OCD co-morbidity require integrated management and genetic counseling when applicable.
  • Public health and safety considerations: botulism is a reportable disease; educate about risks (raw honey in children <12) and exposure sources.