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Flashcards in Medicine - Neuro Deck (73):

Most common parts of the brain affected by lacunar strokes

Lacunar stroke - affect subcortical areas of cerebrum and brainstem. Most commonly basal ganglia, thalamus, pons, and internal capsule.


Most common sites for intracranial hemorrhage 2/2 Hypertensive vasculopathy?

Putamen (44%)
Thalamus (13%)
Cerebellum (9%)
Pons (9%)
Other cortical areas (25%)


Normal cerebral blood flow? (in mL/100g of brain/min)

At what CBF does the brain exhibit physiologic changes in a stroke?

Normal CBF 40-60 mL/100g of brain/min

When CBF drops below 15-18 mL/100g of brain/min, brain loses electrical activity, although membrane integrity and function remain intact.

When CBF <10mL/100g brain/min, membrane failure occurs → ↑ extracellular K and ↑ intracellular Ca → cell death


Territories of the brain supplied by anterior circulation

80% of the brain: optic nerve, retina, fronto-parietal and anterior-temporal lobes.

Supples basal and medial aspects of cerebral hemispheres, extends to anterior 2/3 of the parietal lobe.


Branches of middle cerebral artery and territories they supply?

MCA supplies:
Lenticulostriate branches: putamen, part of anterior limb of internal capsule, lentiform nucleus, external capsule

Main cortical branches: lateral surfaces of cerebral cortex of anterior portion of frontal lobe to posterolateral occipital lobe


Territories of the brain supplied by posterior circulation?

20% of the brain: brainstem, cerebellum, thalamus, auditory/vestibular centers of the ear, medial temporal lobe, visual occipital cortex


Timing for progression of anterior vs posterior circulation strokes?

Anterior circulation strokes may progress w/in 1st 24h.

Posterior strokes may progress for up to 3d.


Where is the lesion?
Pt presenting with: altered mentation, impaired judgement and insight. Presence of primitive grasp/suck reflexes. Paralysis/hypesthesia of lower limb opposite side of lesion. Leg weakness > arm weakness>

Anterior cerebral artery.


Where is the lesion?

Pt with marked motor/sensory disturbance contralateral to the lesion, worse in face/arm than in leg. Motor disturbance almost always accompanied by numbness in same region.

Blindness ipsilateral to lesion.

Middle cerebral artery


Pt with agnosia and aphasia. Where is the lesion?

Middle cerebral artery of DOMINANT hemisphere


Pt unable to process sensory input, such as speech, and thus fails to understand verbal communication.

Wernicke's aphasia (receptive aphasia).

*** Localizes to dominant hemisphere (usually left)


Pt unable to communicate verbally in an effective way, even though understanding may be intact.

Broca's aphasia (expressive aphasia).

*** Localizes to dominant hemisphere (usually left)


Characteristics of posterior circulation strokes?

CN deficits
Cerebellar involvement
Neurosensory tracts
Reticular activating system - mediates consciousness
Visual agnosia (unable to recognize seen objects) and alexia (unable to understand written word)
Visual neglect

*** CROSSED DEFICITS - motor on 1 side and sensory on the other


Signs of vertebrobasilar artery insufficiency?

Vertigo, syncope, diplopia, visual field deficits, weakness, paralysis, dysarthria, dysphagia, spasticity, ataxia, nystagmus


Pt with intracranial hemorrhage with perihematomal edema out of proportion to hemorrhage. What are you concerned for?

Consider hemorrhage into a metastasis or primary tumor.


Findings on CT imaging with early ischemic stroke?

Hyperdense artery sign (acute thrombus in a vessel), sulcal effacement, loss of insular ribbon, loss of gray-white interface, mass effect, acute hypodensity.

*** Only acute hypodensity and mass effect have been shown to be associated with ↑ risk of ICH after fibrinolysis.


BP goals for acute ischemic stroke?

What are BP parameters for tPA?

Withhold antihypertensives unless SBP >220, DBP >120, or MAP > 130.

Goal BP for tPA: <185/110


BP meds in acute stroke?

Labetalol 10-20mg IVP, may repeat x1
Nicardipine infusion 5mg/h, titrate up by 2.5mg/h at 5-15min intervals


Dosing for tPA?

0.9mg/kg IV, max 90mg.

10% given as bolus, followed by 90% by infusion over 60min.


Timing for tPA?

Recommended within 3h of symptom onset.

Inclusion criteria for extending time window from 3h-4.5h: diagnosis of ischemic stroke causing measurable neurological deficit. (Exclusions: >80yo, NIHSS >25, oral AC regardless of INR, h/o DM PLUS prior ischemic cva)

*** American stroke association recommends given w/in 60min of arrival.


BP goals with intracranial hemorrhage?

BP Goal: <160-180 systolic
MAP < 130mmHg


Reversal agents for coagulopathy in intracerebral hemorrhage?

Warfarin: Vitamin K 10mg IV or SQ, FFP 2-4U, PCC (KCentra) 25-50U/kg depending on INR

Dabigatran: Idarucizumab

Apixaban/Rivaroxaban: PCC (Kcentra)


Post-thrombolytic symptomatic intracranial hemorrhage treatment?

Cryoprecipitate (6-8U) for thrombolytic-associated ICH that occurs shortly (0-3h) after alteplase administration. Later ICH (3h-days) is unlikely to be associated with persistent coagulopathy, because fibrinogen depletion following alteplase administration is transient.


Medical therapies aimed at decreasing ICP in patients with intracerebral hemorrhage? (3)

1. Hyperventilation - can be temporizing measure pending more definitive treatment

2. Mannitol - removes fluid from intracranial compartment, thereby reducing cerebral edema

3. Hypertonic saline (3% or 23.4%) as alternative or in combination with mannitol.

Other experimental modalities: barbiturate coma and hypothermia.


What type of seizure?
Abnormal neuronal firing within a confined population of neurons in 1 brain hemisphere, and clinical manifestations tend to reflect the area of electrical activity.

Partial seizures


What type of seizure?
Focal seizure with preserved mental status

Simple focal seizure


What type of seizure?
Focal seizure with some degree of impaired consciousness

Complex focal seizure


What type of seizure?
Abnormal neuro firing throughout BOTH brain hemispheres, always involves alteration of consciousness.

Generalized seizure


What type of seizure?
Starts as focal seizure, progresses to generalized event

Secondarily generalized seizure


Subtypes of generalized seizure:
Brief, dissociative state, often without muscle or postural changes

Absence seizure


Definition of status epilepticus?

Unremitting seizure activity of >5min duration, or recurrent seizure activity without intervening return to baseline mental status.


Seizure 2/2 hyponatremia.


Hypertonic (3%) saline:
2-3mL/kg of 3% NaCl in rapid sequential boluses until seizures stop.


Seizure 2/2 hypocalcemia.


CaCl or CaGluconate - sequential ampules until seizures stop.


Seizure 2/2 salicylate overdose.


Alkalization, hemodialysis for severe cases.

Administer 0.5-1.0 mEq/kg IV bolus, repeat as needed to maintain blood pH 7.4-7.5


Seizure 2/2 TCA overdose.



Administer 0.5-1.0 mEq/kg IV bolus, repeat as needed to maintain blood pH 7.4-7.5


Seizure 2/2 INH overdose.



5g IV (adult) or 70mg/kg (peds)


Seizure 2/2 Eclampsia.



Loading dose 4-6g IV over 15-20min → 1-2 g/h infusion. Monitor for hyporeflexia.


Eye deviated laterally and down. Ptosis. Dilated, non-reactive pupil.

CN lesion?

What if pupil is still reactive?

CN III: Oculomotor nerve - Motor to levator palpebrae, superior rectus, medial rectus, inferior rectus, inferior oblique muscles. Pupillary constriction via parasympathetic fibers to constrictor pupillae and ciliary muscles.

*** Ischemic CN III injury - esp in diabetes - microvascular ischemic injury to nerve → extraocular muscle paralysis but usually spares pupil. Often painful.


Eye unable to deviate laterally and downward. Patient tilting head toward unaffected eye to overcome inward rotation of affected eye.

CN Lesion?

CN IV: Trochlear nerve - motor supply to superior oblique muscle.


Eye unable to move laterally.

CN Lesion?
Biggest concern?

CN VI: Abducens nerve - motor supply to lateral rectus muscle.

Tumors in cerebellopontine angle.

↑↑ ICP: because of its position and long intracranial length, ↑ ICP from any cause may → injury/dysfunction of the nerve.


Most common cause of bilateral CN VII palsy?

Lyme disease.


Abrupt onset of lower motor neuro paresis - developing over 72h, progresses to complete paralysis during 1-7d. Associated ear pain, sensory change on affected side of face, ↓ tearing, overflow of tears on the cheek (epiphora), abnormally acute hearing (hyperacusis), impairment/perversion of taste (dysgeusia)



Bell's Palsy (aka idiopathic facial paralysis).

** Treatment earlier = better outcomes, ideally w/in 24h but recommended for pts who present w/in 7d of symptom onset.

Mild/moderate disease: Prednisolone 50-60mg daily x10d with or without taper.

Severe disease: Prednisolone 50-60mg daily x10 days with or without taper PLUS consider additing valacyclovir 1000mg TID or famciclovir 750 qd x7d.


Unilateral facial paralysis, herpetiform vesicular eruptuion, vestibulocochlear dysfunction.

Ramsay Hunt Syndrome

Same as treatment for severe bell's palsy:

Prednisolone 50-60mg daily x10 days with or without taper PLUS consider additing valacyclovir 1000mg TID or famciclovir 750 qd x7d.


Asymmetrical sensorineural hearing loss + unilateral tinnitus, imbalance, headache, ear fullness, otalgia, facial nerve weakness.


Vestibular Schwannoma (CN VIII)

Tx: surgical removal, ablation with sterotactic radiation therapy.


Diabetic cranial mononeuropathy.

What CN are most commonly affected?


Extraocular muscles


Ischemia 2/2 occlusion of intraneural nutrient artery → injury in core fibers, whereas peripheral nerve fibers are less affected because they are also supplied by collateral vessels. Preserved circumferentially located parasympathetic fibers → pupillary sparing that is found in this syndrome.


Unexplained headache + focal neuro deficit, papilledema, seizure, signs and symptoms of intracranial HTN.

Head CT with cord sign or attenuated vein sign.


Central venous thrombosis -- CT shows hyperdensity of thrombosed sinus (cord sign) or deep vein (attenuated vein sign).

Tx: Systemic AC with LMWH or unfractionated heparin to prevent further clot formation and to promote recanalization.
** Even in patients with intracranial hemorrhage on initial imaging.

Consider catheter-based intervention with thrombolysis with tPA for patients with ↓ LOC, ↑ ICP or rapid neurologic deterioration.


Pt with recurring episodes of neurologic symptoms that rapidly evolve over days and slowly resolve over weeks.

Pt may present with unilateral eye pain with variable degree of central vision loss.

OR spasms of leg/trunk on attempts to stand from seated position. Exaggerated DTRs, clonus. Sx bilateral but asymmetrical. LE > UE.


Multiple Sclerosis

1. To halt progression: interferon-β or glatiramer acetate - antiviral and immunomodulatory actions.
2. For acute exacerbations - Methylprednisolone 250-500mg IV q12h x 3-7d.

** Oral prednisone is not helpful and is associated with potential ↑ in disease flares.


Pt presenting with wrist and finger drop + mild numbness over skin of 1st dorsal interosseus muscle. May also include triceps weakness.



Radial mononeuropathy. (C5-T1 roots)

Tx: Usually spontaneous recovery w/in 6-8 weeks. Splint hand in approx 60° of dorsiflexion


Patient with atrophy of hypothenar muscles. Unable to abduct and adduct all fingers. Unable to flex MCP joints of 4th and 5th digits.

+/- loss of sensation to hypothenar eminence and palmar surface of 4th-5th digits.

How to distinguish between proximal and distal lesions?

Ulnar mononeuropathy (C7-T1 roots).

Sensation is due to superficial sensory nerve which breaks off proximal to guyon's canal, therefore neuropathy involving decreased sensation is more likely 2/2 compression in condylar groove of the elbow.


Pain of fingers of the hand. Clumsy-weak hands, particularly when holding a glass or opening screw-top container.

Decreased sensation of radial aspect of 4th digit, distal palmar tip of the index finger.

Weakness of MCP flexion, thumb opposition/abduction/flexion.

Median mononeuropathy (C5-T1 roots) aka Carpal Tunnel Syndrome


Pt with difficulty ambulating 2/2 inability to flex the knee and flail foot (unable to flex or extend the foot at the ankle)

Sciatic mononeuropathy (L4-S3 roots)

Associated with posterior hip dislocation, any form of penetrating/blunt trauma that cuases formation of buttock hematoma. Other causes: deep gluteal injection, prolonged supine immobilization on a firm surface.


Patient with numbness/dysesthesia over skin of upper lateral thigh.

Lateral femoral cutaneous mononeuropathy (aka meralgia paresthetica) - pure sensory nerve as it passes through or over the inguinal ligament, where it may become entrapped or kinked.

Along with facial nerve neuropathy, it is one of the most commonly reported mononeuropathies associated with HIV infection.


Pt with foot drop due to weakness of dorsiflexion, plus weak eversion of the ankle, strong inversion of the ankle.

Common peroneal mononeuropathy - most commonly 2/2 compression as it winds around fibular neck.


How to differentiate between complete spinal cord syndrome and spinal shock.

Spinal shock - loss of bulbocavernosus reflux, which is a normal cord-mediated reflex that may be preserved in complete cord lesions.


What is lost and retained in complete spinal cord syndrome?

Complete spinal cord lesion - total loss of sensory, autonomic, and voluntary motor innervation distal to the spinal cord level of injury.

Reflex responses mediated at the spinal level, such as muscle stretch (deep tendon) reflexes, may persist, although they also may be absent or abnormal.


Bilateral motor paresis.
Distal muscle groups > proximal muscle groups.

+/- sensory impairment, bladder dysfunction, burning dysesthesias.

Type of lesion?
Mechanism of injury?

Central cord syndrome - affects central gray matter and central portions of corticospinal/spinothalamic tracts.

Most often caused by hyperextension injury - postulated mechanism is squeezing/pinching of the spinal cord anteriorly and posteriorly by inward bulging of ligamentum flavum - most commonly 2/2 falls and MVA.

Results in contusion of the spinal cord, with the central portion being most affected. Common in elders with degenerative arthritis and cervical spinal stenosis.

Prognosis depends on age and degree of injury:
<50yo: 80% regain bladder continence, 90% return to full ambulatory status.

>50yo: 30% regain bladder continence and 50% regain ability to ambulate.


Ipsilateral loss of motor function/propioception/vibration.

Contralateral loss of pain/temp sensation below level of injury.

Type of lesion?
Mechanism of injury?

Brown-Sequard syndrome

Results from anatomic or functional hemisection of the spinal cord.

Usually 2/2 penetrating injury.

May also be seen with compressive/intrinsic lesions. Also reported in association with spinal cord tumors, spinal epidural hematoma, vascular malformations, cervical spondylosis, degenerative disk disease, herpes zoster myelitis, radiation injury, result of spinal instrumentation.


Loss of motor function, pinprick, and light touch below the level of the lesion with preservation of some touch, position, vibratory sensation.

Type of lesion?
Mechanism of injury?

Anterior cord syndrome

Most reported cases follow aortic surgery, but may occur after severe hypotension, infection, MI, vasospasm from drug reaction, aortic angiography.

Anatomic lesion may be caused by cervical hyperflexion injury resulting in cord contusion or by protrusion of bone fragments or herniated cervical disk material into spinal canal.

Rarely 2/2 laceration/thrombosis of anterior spinal artery or major radicular feeding vessel.


Grading of neuromuscular weakness (0-5)

0 - No muscle firing
1 - Muscle fires, but unable to move intended part
2 - Able to move, but not against gravity
3 - Able to move against gravity
4 - Able to move, but not at full strength
5 - Full muscle strength present


Acute/subacute onset of paraplegia, transverse level of sensory impairment, sphincter disturbance. Motor, sensory, urinary disturbances, +/- back pain, low-grade fever.

Weakness progresses to paresis, hypertonia, hyperreflexia, clonus, babinski's response. May include dysautonomias.


Acute transverse myelitis.

Pathogenesis unknown, follows viral infection in approx 30%. Other etiologies includes infectious, autoimmune, indiopathic. Can be seen with CT diseases (lupus, sjogren's, anti-phospholipid syndrome, other mixed-connective tissue diseases).

Treatment: tailored to suspected etiology. No studies supporting steroids. Neuro consult suggested, hospitalization is required.


Pt with sudden, severe excruciating back pain. May be in radicular distribution or extend into flank.
May complain of headache and have nuchal rigidity.

Neuro deficits: extremity numbness, weakness, sphincter dysfunction.


Spinal subarachnoid hemorrhage
Usually 2/2 AV malformation. May also be due to tumors, cavernous angiomas, spontaneous hemorrhage 2/2 anticoagulation.

Tx: Neurosurg consult.


Patient with slowly progressive headache, neck pain, sensory disturbance, gait disorder, lower CN dysfunction. Exacerbated by sneeze/cough/valsalva.

PE with lower limb hyperreflexia, weakness/wasting in UE.

*** Loss of pain/temp in UE with preservation of proprioception and light touch - "Dissociative anesthesia", described in "capelike" distribution over shoulders and arms.


Syringomelia - presence of cavitary lesion within substance of spinal cord. Usually chronic progressive.

*** 90% of patients with syringomelia have Arnold-Chiari I Malformation (projection of cerebellar tonsils and medulla into spinal canal).

May also result from spinal cord trauma (often months-years later) or compressive tumors. It may follow meningitis.



Myelopathy involves spinal cord
Radiculopathy involves nerve roots
Neuropathy involves peripheral nerves
Myopathies involve muscle


Patient presenting with respiratory failure.

History of ptosis, blurred vision, diplopia, dysarthria, dysphagia. More recently reporting easy fatiguability, progressive muscle weakness with repeated activities.

Bedside testing?

Myasthenic crisis in Myasthenia Gravis.

Circulating autoantibodies against ACh receptor on junctional folds on post synaptic membrane → direct blocking of receptor, complement mediated destruction of protein, internalization/degradation of receptors.

Crisis most often precipitated by underlying infection, aspiration, medication changes (stopping anticholinergic, starting med that precipitates weakness).

Bedside: apply eye to ptosis, cooling will decrease symptoms and ptosis will improve.

Tx: Mechanical ventilation with bipap or intubation, aggressive care in ICU + plasma exchange OR immunomodulatory therapy with IVIG.

Cholinesterase inhibitors (pyridotigmine/neostigmine) prolong presence of ACh. Immunosuppressants (corticosteroids, cyclosporine, cyclophosphamide, azathioprine, mycophenolate) for chronic tx.

*** Thymectomy for pts with thymoma can lead to remission or ↓ in medications.


Patient presenting with proximal muscle weakness that improves with use, hyporeflexia, dry mouth.


Lambert-Eaton myasthenic syndrome
50% associated with small cell CA of lung

Autoantibodies → inadequate release of ACh from nerve terminals, affecting both nicotinic and muscarinic receptors.

With repeated stimulation, the amount of ACh in the synaptic cleft increases → ↑ strength.

Tx: treatment of underlying neoplastic disorder, IVIG has been reported as useful.


Bacterial meningitis:
Age <1mo

Common pathogens? (4)
Empiric antibiotics?

Common pathogens:
S. agalactiae (GBS)
E. coli
Listeria monocytogenes
Klebsiella spp.

Amp + Cefotaxime
Amp + aminoglycoside


Bacterial meningitis:
Age 1-23mo

Common pathogens? (5)
Empiric antibiotics?

S. pneumo
Neisseria meningitides
S. agalactiae
H. flu
E. coli

Vanc + 3rd gen cephalosporin (ceftriaxone or cefotaxime)


Bacterial meningitis:
Age 2-50yo

Common pathogens? (2)
Empiric antibiotics?

Neisseria meningitides
S. pneumo

Tx: Vanc + 3rd gen cephalosporin (ceftriaxone or cefotaxime)


Bacterial meningitis:
Age 50+ yo

Common pathogens? (4)
Empiric antibiotics?

S. pneumo
N. meningitides
Listeria monocytogenes
Aerobic GNR (eg pseudomonas)

Tx: Vanc + ampicillin + 3rd gen cephalosporin (Ceftriaxone/cefotaxime)


Bacterial meningitis:
H/o Basilar skull fx

Common pathogens? (3)
Empiric antibiotics?

S. pneumo
H. flu
Group A β-hemolytic strep

Tx: Vanc + 3rd gen cephalosporin (Ceftriaxone/cefotaxime)


Bacterial meningitis:
H/o penetrating trauma

Common pathogens? (3)
Empiric antibiotics?

Staph aureus
Coag-negative staph (esp S. epidermidis)
Aerobic GNR (incl pseudomonas)

Tx: Vanc + cefepime
Vanc + ceftazidime
Vanc + meropenem


Bacterial meningitis:
H/o CSF shunt

Common pathogens? (4)
Empiric antibiotics?

Staph aureus
Coag-negative staph (esp S. epidermidis)
Aerobic GNR (incl pseudomonas)
Propionibacterium acnes

Tx: Vanc + cefepime
Vanc + ceftazidime
Vanc + meropenem


Prophylaxis treatment for meningococcal or Hib meningitis meningitis?
Children > 1mo
Children <1mo

Single dose alternatives?

Rifampin PO q12h x4 doses
Adults: 600mg
Children >1mo: 10mg/kg
Children <1mo: 5mg/kg

Single dose alternatives:
Cipro 500mg PO (adults only)
Ceftriaxone 250mg IM (125mg IM for <15yo)

*** ppx for HIB meningitis is recommended for non-pregnant household contacts when there are children <4yo in the household.