Neuro (8%) Flashcards
Encephalopathy
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)
Epidural hematoma
- 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
Subdural hematoma
- 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)
Hydrocephalus
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
Symptoms of increased ICP
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)
Meningitis
- 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)
Spinal fluid characteristics of bacterial vs. viral meningitis
- 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
Myasthenia gravis
- 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
Guillian-Barre
- 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
Parkinson’s disease
- 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
Epilepsy (everything but treatment)
- 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)
Seizure treatment
- 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.
Tumors
- 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
Autonomic dysreflexia
- 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
Brown-Sequard syndrome
- 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
Central cord syndrome
- 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
Subarachnoid hemorrhage
- 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
Ischemic stroke
- 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
Absolute contraindications to TPA for ischemic stroke
- 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
NIHSS stroke scale scores
- < 4 = good prognosis, no TPA
- 4-20 = mild to moderate stroke, idea TPA candidate
- > 20 = severe deficit, no TPA
Traumatic brain injury (everything except treatment)
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
Traumatic brain injury management
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
Primary vs. secondary headache
- 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.
Headache “red flag” symptoms
- 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)
Primary headache treatment
- 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)
Cluster headache
- 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
