Neuro (8%) Flashcards

1
Q

Encephalopathy

A

 Delirium and acute confusional state during an acute condition of cerebral dysfunction in the absence of structural brain disease
 Manifestations – non-specific/based on etiology – impaired attention, decreased alertness, hallucinations, seizures, tremor, disturbed sleep-wake cycle
 Treatment – treat underlying condition, review MAR, discontinue meds with CNS toxicity, fall precautions, restraints (last resort)

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2
Q

Epidural hematoma

A
  • Rapid accumulation of blood from an ARTERIAL source between the dura mater and the skull
  • Can be caused by fractures to the temporal or parietal skull and/or injury to the middle meningeal artery
  • Often a “lucid interval” where patients have few symptoms then progressive neurologic deterioration
  • Manifestations – headache, transient LOC, unilateral fixed or dilated pupil is classic, n/v, dizziness
  • Diagnostic – CT of head
  • Treatment – surgical intervention if significant, BP control
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3
Q

Subdural hematoma

A
  • Damage to the bridging VEINS causing blood to accumulate under the dura mater
  • Can be acute or chronic
  • Common in elderly and those with etoh abuse
  • Manifestations – headache, gradual LOC/change in mental status, seizures
  • Treatment – surgical intervention if significant, watch and weight, anti-seizure prophylaxis for 7 days (most patients will fall into the “watch and wait” category)
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4
Q

Hydrocephalus

A

 Disorder in which an excessive amount of CSF accumulates
 Obstructive and communicating hydrocephalus are mainly seen in children
 Normal pressure hydrocephalus is most common in adults
 Etiology – intraventricular and/or subarachnoid hemorrhage, meningitis, Paget disease
 Manifestations – 3 cardinal features – gait difficulty (most prominent, “magnetic gait”, short steps), cognitive disturbances (decreased attention, concentration), and urinary incontinence
 Diagnostics – MRI is test of choice
 Treatment – shunting (VP or VA) if suitable

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5
Q

Symptoms of increased ICP

A

 Early – headache, n/v, change in mental status/LOC, change in behavior
 Late – unresponsive, dilated or non-reactive pupils, posturing, Cushing’s triad (bradycardia, widened pulse pressure, and apnea)

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6
Q

Meningitis

A
  • Infection of the pia pater and the arachnoid mater of the brain
  • May be infectious, chronic, or aseptic
  • Manifestations – severe headache, nuchal rigidity, high fever, AMS, Kerning’s sign (patient supine, pain elicited by passive extension of knee), Burdzinski’s sign (flexion of neck causes flexion of hip and knee)
  • Diagnostics – LP as soon as diagnosis is suspected (CT scan first to rule out space-occupying lesion)
  • Treatment – high-dose parenteral antibiotics if purulent suspected (bacterial), may need dexamethasone (can help with inflammation)
  • Antibiotics – 3rd generation cephalosporin (ceftriaxone, ceftazidime)
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7
Q

Spinal fluid characteristics of bacterial vs. viral meningitis

A
  • Bacterial (purulent) – cell count: 200-200,000; glucose < 45; protein >50 (usually very high); markedly high opening pressure
  • Viral – cell count: 100-1,000; normal glucose (50-80); protein > 50 (but < purulent); normal opening pressure
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8
Q

Myasthenia gravis

A
  • Autoimmune dysfunction of acetylcholinesterase
  • Often insidious but often “unmasked” by infection that leads to exacerbation
  • Manifestations – muscle weakness (typically descending) that worsens with activity and improves with rest; fluctuating muscle weakness; fatigue with chewing
  • Diagnostics – serum acetylcholine receptor antibodies (AChR), EMG studies
  • Treatment – acetylcholinesterase inhibitors (mestinion – titrate to 60-120 mg every 3-4 hours), prednisone, plasmapheresis, IVIG
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9
Q

Guillian-Barre

A
  • Acute inflammatory polyneuropathy/paralyzing illness provoked by infection, inoculation, or surgery
  • Manifestations – begins in lower extremities and ascends bilaterally, weakness, ataxia, bilateral paresthesia progressing to paralysis
  • Diagnostics – CSF has high protein concentration; EMG shows delayed conduction; spirometry monitor q6h
  • Treatment – NO STEROIDS, admit to ICU for supportive care (intubate if needed), IVIG 400 mg/kg/day x5 days
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10
Q

Parkinson’s disease

A
  • A degenerative CNS disorder resulting from an imbalance of dopamine and acetylcholine
  • Manifestations – resting tremor, rigidity, bradykinesia, “pill rolling”, can progress to impaired swallowing and decreased autonomic movement
  • Management – pharmacologic options focus around increasing amount of dopamine – Carbidopa-Levodopa (Sinemet) is gold standard and average duration of response to med is 5 years; Selegiline is another option
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11
Q

Epilepsy (everything but treatment)

A
  • Person has recurrent seizures d/t chronic, underlying process, 2 or more unprovoked seizures
  • Etiology – non-compliance with meds (#1), most seizures in ICU are provoked and not considered epilepsy (electrolyte disturbances, cerebral edema, infection, drugs, etc.)
  • Focal seizure – one hemisphere; can be simple (remain conscious) or complex (altered consciousness, but not loss)
  • Generalized – both hemispheres; convulsive (tonic-clonic with loss of consciousness) or non-convulsive (typical has automatisms [lip smacking, blinking, chewing or atypical is absence)
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12
Q

Seizure treatment

A
  • Immediate resolution of seizures – lorazepam 2mg IVP, max 10 mg
  • Treat/correct underlying cause
  • Antiepileptic drug therapy (AED) is individualized – phenytoin, levetiracetam (Keppra), valproic acid, etc.
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13
Q

Tumors

A
  • Earliest sign of tumor – ipsilateral pupillary dilation
  • Glioblastoma – most common cause of malignant primary brain tumor, treatment = surgery, chemo, radiation
  • Meningioma – common primary brain tumor; s/s = headache, seizure, focal neuro deficits; treatment depends on size – surgical resection
  • Primary adenoma – hormone hypersecretion, visual impairment, headaches; treatment – transphenoidal surgery
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14
Q

Autonomic dysreflexia

A
  • Injury location – above T6
  • Cause – traumatic injury
  • Symptoms – exaggerated autonomic responses – above level of injury has diaphoresis and flushing; below level of injury has chills and vasoconstriction; other symptoms include HTN, bradycardia, headache
  • Treatment – remove stimulus/treat injury, manage autonomic manifestations
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15
Q

Brown-Sequard syndrome

A
  • Injury location – anywhere along the cord
  • Cause – penetrating trauma (“cut” halfway through the cord)
  • Symptoms – ipsilateral (same side) motor disturbance; contralateral loss of pain and temperature sense
  • Treatment – immobilization, transfer to trauma, steroids
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16
Q

Central cord syndrome

A
  • Injury location – cervical spinal cord
  • Cause – hyperextension injury
  • Symptoms – upper and lower extremity weakness (more in upper); varying degree of sensory loss below level of injury
  • Treatment – ICU monitoring for 24 hours; monitor for autonomic dysreflexia, HTN, and bradycardia; usually resolves on own; most are mild and self-limiting
17
Q

Subarachnoid hemorrhage

A
  • Bleeding into the subarachnoid space secondary to cerebral aneurysm or head injury
  • Rapid accumulation of blood from ARTERIAL source
  • Most common causes are uncontrolled HTN or vascular malformations
  • Manifestations – thunderclap headache, “worst headache of my life”, vomiting, confusion/LOC, seizures
  • Treatment – surgical intervention, BP control; SBP goal 120-160; nimodipine for BP control and vasospasm, cardene IV is SBP> 160
18
Q

Ischemic stroke

A
  • The most important historical component is the time of symptom onset
  • Obtain a history to rule out conditions that mimic stroke (ex: hypoglycemia, OD, infection, etc.)
  • Manifestations – sudden numbness or weakness, confusion, difficulty speaking, trouble seeing, dizziness, severe headache without cause
  • All patients should have a head CT or MRI, ECG, and labs
  • Most patients with HTN will demonstrate a decrease in BP after a few hours without intervention
  • If patient is a candidate for tPA, BP reduction should be done if SBP > 220 or DBP > 110
  • TPA needs to be started within 4.5 hours of symptom onset
19
Q

Absolute contraindications to TPA for ischemic stroke

A
  • Current intracranial bleeding
  • Subarachnoid hemorrhage
  • Active internal bleeding
  • Recent intracranial or intra-spinal injury or serious head trauma < 3 months ago
  • Bleeding diathesis
  • Current severe uncontrolled HTN
20
Q

NIHSS stroke scale scores

A
  • < 4 = good prognosis, no TPA
  • 4-20 = mild to moderate stroke, idea TPA candidate
  • > 20 = severe deficit, no TPA
21
Q

Traumatic brain injury (everything except treatment)

A

 Non-generative, non-congenital insult to the brain from an external mechanical force leading to permanent or temporary impairment of function
 Can be primary (from injury itself) or secondary (a consequence of injury – cerebral edema, increased ICP, ischemia, etc.)
 Severity scores – GCS – mild (GCS 13-15), moderate (GCS 9-12), severe (GCS ≤ 8)
 ABCDE initial surgery
 Neuroimaging – head CT

22
Q

Traumatic brain injury management

A

 Oxygenation
 Maintain euvolemia and frequent labs to check electrolytes
 DVT prevention (caution, risk for hemorrhagic conversion is highest in first 24-48 hours)
 If ICP > 20 – HOB to 30 degrees, monitor CVP, CSF removal 1-2 ml/min for no greater than 3 minutes at a time, Mannitol bolus 0.25-1 g/kg q4-6h PRN
 Seizure prophylaxis – Keppra, valproic acid, or phenytoin for 7 days
 CPP (CPP = MAP – ICP) should be ≥ 60 to ensure adequate brain perfusion
 Inpatient rehab is most common form of rehab for severe TBI patients

23
Q

Primary vs. secondary headache

A
  • Primary – not associated with other disease; ex: migraines, tension-type, cluster
  • Secondary – associated with or caused by other conditions; ex: tumor, intracranial bleeding, increased ICP, etc.
24
Q

Headache “red flag” symptoms

A
  • SNOOP
  • S – systemic symptoms – fever, weight loss
  • N – neurologic signs – new neuro finding, confusion, impaired alertness, etc.
  • O – onset (time) – sudden, abrupt, “thunderclap”; onset with exertion, sexual activity, coughing, etc.
  • O – onset (age) – older > 50 years, younger < 5 years
  • P – prior headache hx (change in quality or frequency), positional, papilledema (visual problems)
25
Q

Primary headache treatment

A
  • Lifestyle modification – recognize and avoid triggers, regular exercise, correct posture, etc.
  • Analgesics – NSAIDs, acetaminophen (limit use to 2 treatment-days per week)
  • Rescue therapy – when standard therapy ineffective or specific symptoms are present– opioids, antiemetics, short course of corticosteroids
  • Migraine-specific meds – the “-tripans”, caution in pregnancy and uncontrolled HTN
  • Prophylactic (controller) meds – beta blockers (propranolol), TCAs (amitriptyline), anti-epileptic drugs (gabapentin)
  • Indication for prophylaxis – use any product > 3x/week, ≥ 2 migraines/month that produce severe symptoms ≥ 3 days, poor symptom relief with abortive therapies, presence of concomitant medical conditions (ex: HTN)
26
Q

Cluster headache

A
  • Headaches occur daily in groups or clusters and last several weeks to months and then disappear
  • Typically located behind 1 eye with a steady, intense, “hot poker in the eye” sensation
  • Often has ipsilateral autonomic signs such as lacrimation, conjunctival injection, and nasal stuffiness