NS LM3 cheat sheet

Central nervous system = brain + spinal cord; peripheral nervous system = cranial nerves (12 pairs), spinal nerves (31 pairs), and autonomic ganglia.

Neuron parts: dendrites receive, soma integrates, axon conducts, axon terminal releases neurotransmitter across the synaptic cleft.

Resting membrane potential is about -70 mV, maintained by Na+/K+-ATPase pumping 3 Na+ out for every 2 K+ in.

Action potential sequence: threshold (~-55 mV) → Na+ influx depolarization → K+ efflux repolarization → brief hyperpolarization → return to rest.

Myelination by oligodendrocytes (CNS) and Schwann cells (PNS) enables saltatory conduction and faster velocity; demyelination slows or blocks conduction.

Neurotransmitter removal occurs by reuptake, enzymatic degradation, or diffusion; SSRI and SNRI drugs block serotonin/norepinephrine reuptake.

Sympathetic activation: increased heart rate, mydriasis, bronchodilation, decreased peristalsis; parasympathetic (vagus) does the opposite.

Blood-brain barrier is formed by tight junctions of capillary endothelial cells, astrocytes, and pericytes; it excludes many polar drugs and large molecules.

Cerebrospinal fluid is produced mainly by choroid plexus at roughly 500 mL/day; total volume is about 150 mL and is replaced about 3-4 times daily.

Frontal lobe: motor cortex, Broca area (expressive speech, dominant hemisphere), executive function, and personality.

Parietal lobe: primary somatosensory cortex; right parietal lesions cause contralateral neglect.

Temporal lobe: primary auditory cortex, Wernicke area (receptive language, usually left), and hippocampus for memory consolidation.

Occipital lobe: primary visual cortex; lesions produce homonymous visual field deficits.

Cerebellum: coordination, balance, and error-based motor learning; lesions cause ipsilateral ataxia, dysmetria, intention tremor, and nystagmus.

Basal ganglia (caudate, putamen, globus pallidus, substantia nigra, subthalamic nucleus): movement initiation and modulation; dopamine loss in substantia nigra produces Parkinsonism.

Brainstem: midbrain (CN III-IV), pons (CN V-VIII), medulla (CN IX-XII); medulla contains respiratory and cardiac centers.

Corticospinal tract decussates in the medulla, so upper motor neuron lesions cause contralateral weakness; cranial nerve and spinal nerve signs help localize.

Limbic system (amygdala, hippocampus, cingulate) mediates emotion, fear, and memory; thalamus relays sensory input except olfaction.

Glasgow Coma Scale: eye 1-4, verbal 1-5, motor 1-6; total 3-15; score ≤8 indicates severe impairment and airway risk.

Pupillary light reflex: CN II afferent, CN III efferent; fixed dilated pupil suggests CN III compression (uncal herniation).

Cranial nerve screen order: I smell, II vision, III/IV/VI eye movements and pupils, V facial sensation and masseter, VII facial movement, VIII hearing, IX/X swallow and gag, XI shoulder shrug, XII tongue.

Motor exam grades 0-5: 0 no contraction, 1 trace, 2 movement without gravity, 3 against gravity, 4 against resistance, 5 normal.

Deep tendon reflexes graded 0-4+; 2+ is normal; hyperreflexia suggests upper motor neuron lesion, areflexia suggests lower motor neuron or peripheral nerve lesion.

Babinski sign: dorsiflexion of great toe with fanning indicates upper motor neuron lesion in adults.

NIH Stroke Scale scores 0-42; higher scores indicate greater deficit; note time of symptom onset (last known well) for treatment decisions.

Decorticate posturing (flexor arms, extensor legs) indicates lesion above the red nucleus; decerebrate (extensor arms and legs) indicates lower brainstem lesion and is worse.

Delirium features acute onset, fluctuating course, and inattention; assess with a validated tool such as the Confusion Assessment Method.

Ischemic stroke: sudden focal deficit; thrombolysis window generally up to 4.5 hours from last known well; thrombectomy may extend to 24 hours in selected large-vessel occlusion.

Hemorrhagic stroke: sudden severe headache, vomiting, hypertension; confirmed by non-contrast CT; avoid thrombolytics and anticoagulants.

Seizure vs status epilepticus: status epilepticus is continuous seizure ≥5 minutes or repeated seizures without recovery; first-line is a benzodiazepine.

Migraine: unilateral pulsating headache with photophobia, nausea, and aura in some patients; treated with triptans or NSAIDs; preventive agents include beta-blockers and topiramate.

Multiple sclerosis: demyelinating plaques disseminated in time and space; common symptoms include optic neuritis, diplopia, paresthesias, and fatigue.

Parkinson disease: resting tremor, bradykinesia, rigidity, and postural instability; caused by loss of dopaminergic neurons in the substantia nigra.

Myasthenia gravis: fatigable weakness, ptosis, and diplopia due to antibodies against acetylcholine receptors at the neuromuscular junction.

Guillain-Barré syndrome: ascending symmetric weakness with areflexia after infection; monitor vital capacity because respiratory failure can occur.

Increased intracranial pressure: headache, vomiting, papilledema, decreased consciousness; Cushing triad (hypertension, bradycardia, irregular respirations) is a late sign.

Non-contrast head CT is first-line for acute stroke to exclude hemorrhage; it detects acute hemorrhage immediately but early ischemia may not be visible.

MRI is more sensitive than CT for acute ischemia, demyelination, and posterior fossa lesions; contraindicated with certain implanted metal or pacemakers.

CT angiography identifies large-vessel occlusion and aneurysm; CT perfusion identifies salvageable penumbra in extended-window stroke.

Lumbar puncture: opening pressure normal 10-20 cm H2O; bacterial meningitis shows elevated white cells with neutrophil predominance, high protein, low glucose.

Lumbar puncture is contraindicated with signs of raised intracranial pressure or coagulopathy because of herniation risk.

EEG detects seizure activity and status epilepticus; routine EEG is brief, while continuous EEG monitors nonconvulsive seizures.

Electromyography and nerve conduction studies distinguish myopathy (myopathic units) from neuropathy (reduced conduction velocity, denervation).

Carotid Doppler ultrasound screens for stenosis; digital subtraction angiography remains the reference standard for vascular anatomy.

Serum tests useful in neurology include TSH, B12, glucose, electrolytes, and toxicology; CSF analysis includes cell count, protein, glucose, Gram stain, and culture.

Acute ischemic stroke thrombolysis: alteplase or tenecteplase; exclude hemorrhage, uncontrolled hypertension (>185/110 mmHg), and recent surgery before giving.

Antiepileptic drugs: levetiracetam, phenytoin, valproate, and lamotrigine; monitor levels for phenytoin and valproate; teratogenicity limits valproate in pregnancy.

Parkinson disease: levodopa/carbidopa is most effective; carbidopa blocks peripheral decarboxylation to reduce nausea and increase brain delivery.

Dopamine agonists (pramipexole, ropinirole) and MAO-B inhibitors (selegiline) are alternatives or adjuncts in Parkinson disease.

Multiple sclerosis: high-dose corticosteroids for acute relapse; disease-modifying agents reduce relapse rate; natalizumab carries progressive multifocal leukoencephalopathy risk.

Myasthenia gravis: pyridostigmine (acetylcholinesterase inhibitor) for symptoms; immunosuppressants for maintenance; avoid aminoglycosides and other agents that worsen weakness.

Migraine: triptans are contraindicated with coronary artery disease and uncontrolled hypertension; ergotamines are contraindicated in pregnancy.

Mannitol and hypertonic saline are osmotic agents used for raised intracranial pressure; monitor serum osmolality and renal function.

Opioids and sedatives depress respiratory drive and mask neurologic deterioration; naloxone reverses opioids; flumazenil reverses benzodiazepines.

Aspiration precautions: keep head of bed elevated 30-45 degrees, screen swallowing before oral intake after stroke, and use thickened liquids if indicated.

Fall prevention: bed low and locked, call light within reach, non-skid footwear, and assistance with ambulation for patients with ataxia or weakness.

Seizure precautions: padded side rails, suction and oxygen at bedside, do not restrain during seizure, protect head, and time the event.

A patient with new confusion, unequal pupils, or decreasing consciousness requires urgent notification of the provider for possible herniation.

Thrombolytic safety: monitor for bleeding, avoid invasive procedures and urinary catheter placement for a period after administration per protocol.

Documentation must record time of symptom onset (last known well), neurologic assessments, interventions, and responses.

Scope of practice: administer and monitor medications per orders and institutional policy; report adverse effects and errors through the appropriate reporting system.

Infection control: hand hygiene and standard precautions; patients with altered immunity or recent neurosurgery require vigilance for meningitis signs.

Communication: use structured handoff (e.g., SBAR) and confirm patient understanding with teach-back for discharge instructions.