Neurological Emergencies · CVA e. Complex/complicated migraine/migrainous infarction i. Aura lasting 7 days ii. Can show infarction by MR/CT 4. Treatment: Abortive therapies; What

Neurological Emergencies

Henry Pitzele, MD, FACEP

Associate Director, Section of Emergency Medicine, Jesse Brown VA Medical Center, Chicago; Clinical Assistant Professor, Department

of Emergency Medicine, University of Illinois at Chicago

Notes

Neurological Emergencies Page 1

NEUROLOGICAL EMERGENCIES

I. HEADACHE

A. Common: 4% of ED visits

B. 40% of Americans with lifetime serious HA

C. Wide-ranging causes

1. Primary (90%) a. Migraine b. Cluster c. Tension

2. Secondary a. Vascular b. Traumatic c. Space-occupying d. Inflammatory e. Miscellaneous

D. Migraine

1. General

a. Common (1M/yr) but often misdiagnosed b. 3:1 F:M ratio c. Often in children, but peaks at age 40 d. Symptoms often oscillate with menstrual cycle e. Family history sometimes present

2. Pathophysiology a. Previously thought to be vasospastic/vasodilatory b. Now, more complex theory:

i. Trigger ii. Primary neuronal dysfunction/hypoactivity iii. Vascular constriction follows neuronal hypoactivity iv. Sensory axons activated, release peptides v. Induce HA (sterile neurogenic inflammation)

3. Presentation: differs by clinical migraine syndrome a. Migraine without aura (common migraine)

i. Unilateral, pulsating, slow onset ii. Last 4-72h iii. N/V, phono- and photophobia

b. Migraine with aura (classic migraine) i. Prodrome: gradual onset, lasting <60 min, fully

reversible ii. Often visual (scintillating scotomata), but iii. Aura can be ANY focal neuro defect

Notes


c. Ophthalmoplegic migraine i. Transient or permanent paresis of III (occas IV or VI) ii. Can be mimicked by expanding Berry aneurysm

d. Hemiplegic migraine i. Unilateral motor or sensory deficit as aura ii. Occas, aura outlasts symptoms—may actually be

CVA e. Complex/complicated migraine/migrainous infarction

i. Aura lasting 7 days ii. Can show infarction by MR/CT

4. Treatment: Abortive therapies; What has worked for patient in

the past? Severity based stratification / Stepwise approach a. Mild to moderate

i. PO Tylenol / NSAID / ASA ii. IV/IM metoclopramide helps efficacy (gastroparesis)

b. Mod to severe: i. Prochlorperazine (Compazine) 10 IVS Side: EPS ii. Metoclopramide (Reglan) 10 IV. Side: Dystonia iii. Ketorolac (Toradol) 30 IV; Avoid in elderly, CRI,

GIB Hx c. Severe (migraine-specific)

i. DHE (dihydroergotamine) 1.0 mg IV • Co-administer with antiemetic • Contra: preg, CAD, Imitrex < 24h prior

ii. Sumatriptan (Imitrex) 6 SQ • Contra: preg, CAD, MAOI, DHE < 24h

d. Not unless you ABSOLUTELY have to: i. Meperidine (Demerol) 50 IM / IV

e. Steroids: Too controversial for this test 5. Treatment: preventive

a. Many classes used in past—B Blocker, Tricyclic, CCB b. Not recommended for start in ED

E. Cluster

1. Unique syndrome distinct from migraine 2. More common in males 3. Average age at onset is 30 years 4. Short-lived headaches (lasting 20 minutes to 3 hours)

occurring in clusters one to four times in 24 hours, and can occur for several weeks at a time

5. Pain is severe, ipsilateral, retroocular, with patients usually pacing the floor, rocking, holding head

6. Distinct autonomic symptoms: nasal stuffiness, lacrimation, Horner’s Syndrome, all ipsilateral

7. Pathophysiology: not well understood. May be related to histamine release from mast cells

Notes


8. Treatment

a. (Abortive) 100% oxygen i. Similar to other migraine treatment (Imitrex first line) ii. Some suggest installation of cocaine or lidocaine into

ipsilateral nostril b. (Preventive) Lithium, Prednisone

F. Muscle/tension

1. Probably the most common form of headache but be wary of

making this diagnosis before more serious etiologies are ruled out

2. Pathophysiology: Previously thought due to contraction of frontal and occipital muscles, exacerbated by stress, depression, lack of sleep. Now thought to be on same continuum as migraine

3. Presentation: Usually localized to front-temporal or cervico-occipital areas, spreading to shoulders. Usually gets worse as the day progresses. Usually bilateral

4. Diagnosis: By exclusion, after ruling out other causes 5. Management: NSAIDS, as well as acetaminophen or

salicylates. Severe tension treated same as migraine. Butalbital-containing drugs (e.g., Fiorinal) may be helpful in short course

G. Cavernous sinus and dural sinus thrombosis

1. Pathophysiology: Dural sinuses drain the brain, and infection

of sinuses or mastoid lead to thrombophlebitis 2. Presentation: Cavernous sinus thrombosis is usually secondary

to infections of ethmoid, sphenoid, or maxillary sinuses. Clinically, see headache, fever, seizure, cranial palsies, papilledema, chemosis, proptosis, ptosis. Lateral sinus thrombosis usually from middle ear or mastoid infection.

3. Diagnosis: Enhanced CT or MRI; angiogram may be needed 4. Treatment: Antibiotics; consider anticoagulation

H. Traumatic causes

1. Subarachnoid hemorrhage 2. Subdural hematoma 3. Intracerebral hemorrhage 4. Epidural hematoma

I. Space-occupying

1. Mass lesions

Notes


a. Headaches from tumor are notoriously variable in presentation. Typical pattern in headache: worse in the morning, subtle personality changes, sleep disturbance, nausea and vomiting. Suspect in patients with prior history of malignant tumors that metastasize to CNS.

b. Diagnosis: Either CT with contrast or MRI with gadolinium

c. Treatment: Prompt neurologic/neurosurgical consultation d. Decadron often used to decrease edema surrounding mass

2. Pseudotumor cerebri (benign/idiopathic intracranial hypertension) a. Unusual, but suspect in younger, obese females b. Clinically: recurrent headaches, some with visual

disturbances, nausea and vomiting, irregular menses, papilledema or EOM disturbance on exam with normal level of consciousness

c. Diagnosis: CT scan shows slit-like, narrow ventricles from elevated ICP; increased opening pressure on LP (200-500 mm H20)

d. Treatment: Therapeutic LP, acetazolamide, steroids

J. Inflammatory headaches

1. Temporal arteritis a. Pathology: granulomatous vasculitis affecting large and

medium-sized arteries b. Epidemiology: typically in the elderly (60-80 years old,

almost never before 50 y.o.), more common in females c. Symptoms: severe persistent headaches, tender and

pulseless temporal artery, visual loss, malaise, polymyalgia rheumatica (myalgias of back, shoulders, extremities), jaw claudication

d. Diagnosis: sedimentation rate over 50 (usually at least 100), temporal artery biopsy; DON’T DELAY TREATMENT WHILE WAITING FOR BIOPSY

e. Treatment: steroids, usually Prednisone 50-100 mg/day for one month, followed by a slow taper over 6 months

2. CNS infections a. Meningitis, encephalitis, brain abscesses can all present

with headache-sometimes a mild form. See sections on CNS infections

3. Post-traumatic a. Covered in neurotrauma lecture

K. Miscellaneous causes of headache

1. Trigeminal neuralgia - unilateral severe facial pain in lips,

gums, cheek, chin; occurs in sharp, lightening-like bursts; often

Notes


triggered by stimuli talking or eating; painless in between paroxysms a. Usually presents after age 40 (if younger, think of

differential diagnosis of multiple sclerosis, TMJ pain) i. Neuro exam should be normal ii. CT or MRI should be done to rule out structural

lesions mimicking or triggering trigeminal neuralgia b. Treatment: medications (Carbamazepine, Baclofen,

Amitriptyline) treat most patients. Acutely, may need parental analgesia. Resistant cases may need surgical decompression of nerve roots.

2. Glaucoma a. Suspect in elderly or African-American patient with severe

headache and visual complaints, eye pain 3. Carbon monoxide

a. Non-specific headache, often with flu-like symptoms b. Ask if others in environment with similar symptoms

4. Post-LP headache a. Occurs within 24-48h in up to 40% of LPs b. Symptoms are usually positional, occurring upon standing,

relieved by supine position c. Thought to be due to persistent dural leak and subsequent

CSF hypotension d. Treatment with analgesics, and IV fluids and caffeine

Refractory cases managed with autologous epidural blood injection (blood patch)

II. CNS INFECTIONS

A. Meningitis

1. Meningitis is a neurological emergency that can present in everyday practice. Prompt diagnosis and treatment can seriously affect outcome, and a high index of suspicion is always warranted

2. The mortality of untreated bacterial meningitis exceeds 90%; with aggressive therapy, mortality decreases to 10-20%

3. Etiologies include bacterial, viral, chemical, or neoplastic 4. Clinically - symptoms alone cannot help distinguish bacterial

from viral cause a. Physical findings include: headache, fever, stiff neck,

vomiting (classic presentations) but be aware of others: seizure, altered mental status, focal neurologic deficits. Remember: the very young and the very old can present with few and subtle symptoms. Again, high index of suspicion for extremes of age, the immunocompromised, alcoholics, nursing home patients.

Notes


i. Look for papilledema, focal deficits ii. Check for Kerning’s sign (pain on passive extension

of the knee with hips flexed) iii. Brudzinski’s sign (flexion of hips and knees with

passive neck flexion) iv. Look for rash--petechial or purpuric rash of

meningococcemia v. Other sources of infection including ears, sinuses, etc.

b. Treatment i. Initiation of treatment is the key element. A good rule

of thumb is: DO NOT WAIT FOR ANYTHING. Don’t wait for consultants, CT scan results, or anything that will come between your patient and treatment

ii. If increased intracranial pressure is suspected due to papilledema or focal neurologic deficit, get head CT prior to LP. However, START ANTIBIOTICS prior to patient going to CT

iii. Empiric therapy should be given before LP results are back if patient appears toxic

iv. Treatment is based on presumed agents of infection for given age group or type of patient

v. Neonates: E. Coli, group B streptococci, Listeria, Pseudomonas

vi. Children: pneumococcus, meningococcus (H. flu) vii. Older children and adults: pneumococcus,

meningococcus, (rarely H. flu) viii. Special groups

• Alcoholics: pneumococcus, listeria, gram negatives

• Immunocompromised: gram negatives, fungal • Shunt patients: coagulase- negative

staphylococci • Splenectomized patients: pneumococcus, H. flu,

staph • AIDS patients: cryptoccocus

ix. Results of lumbar puncture • Classically in bacterial meningitis: elevated WBC

counts (greater than 500) with PMN predominance, elevated protein, and decreased glucose. Viral causes typically have lower WBC counts with lymphocytic predominance.

• Other diagnostic methods •• Latex agglutination: fairly quick to assess H.

flu Pneumococcus, N. meningitidis. Useful in partially treated meningitis.

•• Gram stain: helpful only if positive •• Cryptococcal antigen in

Notes


immunocompromised, AIDS patients •• Acid-fast stain for mycobacteria

c. Empiric antibiotics i. Neonates: Ampicillin and Gentamicin or

Ampicillin and Cefotaxime. • Infants to 3 years: Ceftriaxone (or other third

generation cephalosporin) or Amp and chloramphenicol

ii. Immunocompetent adults: Ceftriaxone plus vancomycin (for S. pneumoniae resistance) • Over 50 years: Ceftriaxone plus Ampicillin plus

Vancomycin (for S. pneumoniae resistance) iii. CSF leak/closed head injury: ceftriaxone iv. CSF shunt, neurosurgery, penetrating head injury:

• Vancomycin plus Ceftazidime v. Immunocompromised:

• Vancomycin plus Ampicillin plus Ceftazidime • AIDS patients with +cryptococcal Ag on CSF:

consider amphotericin d. Steroids—give them! Dexamethasone 10 mg before first

antibiotic.

B. Encephalitis

1. Encephalitis presents with altered state of consciousness, impaired cognitive abilities, and CSF pleocytosis. Patients can present in a similar fashion to bacterial/viral meningitis: a. Altered mental status b. Range of mental status from lethargic to comatose c. Can present afebrile, with new psychiatric condition or

neuro deficit d. Look for non-CNS syndromes as evidence of causative

virus 2. Etiology: mostly viral, such as Herpes simplex (HSV),

arbovirus (RNA viruses causing St. Louis encephalitis, West Nile Virus, eastern and western equine encephalitis, etc; transmission via arthropods or mosquitos), entero viruses, varicella, HIV, EBV, measles, mumps, rabies. Also caused by mycoplasma, Toxoplasma, Borrelia burgdorferi, and multiple other agents. a. HSV has predilection for temporal and frontal lobes, so

see temporal symptoms of olfactory hallucinations, speech difficulties

b. Seizures are fairly common, especially with HSV: check for cranial nerve palsies, focal deficit

3. Diagnosis a. CT of head to rule out structural lesions, SAH (Note:

Notes


contrast-enhancing ring lesions seen with Toxoplasma/ abscess)

b. MRI playing increasing role c. Lumbar puncture shows a pleocytosis with lymphocytic

predominance; protein modestly elevated, and glucose normal

d. Culture CSF for viruses, bacteria, fungi; check CSF antigen titers for cryptococcus, toxoplasma, and PCR for HSV

e. NOTE: HSV has characteristics RBCs in CSF from necrotic tissue (up to 500 RBCs may be seen)

4. Treatment a. Supportive care b. Clinically key point -- treat for presumptive bacterial

meningitis early in presentation. Give antibiotics as soon as possible.

c. Specific antiviral: acyclovir for HSV. CSF pleocytosis and elevated protein in an encephalopathic patient without clear pathogen is highly suspicious for HSV.

C. CNS abscess

1. Maintain a high index of suspicion for brain abscess as

symptoms overlap those of meningitis and encephalitis. Epidural abscess sometimes presents without fever OR back pain

2. Etiology a. Most common source is direct seeding from otic, nasal,

sinus infections. Less common causes are hematogenous spread or open CNS trauma

b. Organisms - staph, anaerobic and aerobic strep. Other anaerobes, such as Bacteroides

3. Presentation a. Most commonly headache b. Also fever, seizures, focal deficits, signs of increased

ICP Spinal abscess can cause cord compression symptoms

c. Watch for original (seeding) infection 4. Diagnosis

a. CT of head with contrast; MRI, especially in epidural/spinal location

b. Lumbar puncture contraindicated due to risk of herniation

5. Treatment a. Neurosurgical consultation b. Empiric coverage with Penicillin and Ceftriaxone +/-

Metronidazole. (Nafcillin +/- Vanco if staph suspected; if pseudomonas suspected, can add Ceftazidime and/or

Notes


gentamicin; AIDS patients with cerebral toxoplasmosis receive pyrimethamine and sulfadiazine)

III. CNS TUMORS

A. CNS tumors are an important cause of neurologic complaints, and a high index of suspicion in the emergency department is necessary for several reasons.

B. They occur with often subtle presentations. Prompt diagnosis and

treatment may be necessary to prevent raised intracranial pressure 50% primary tumors, 50% mets, usually from lung, breast, colon, kidney, testicle, melanoma.

C. Cerebral herniation

1. Pathophysiology: Cranium has a limited volume, filled with

three elements: brain, CSF, and blood. An increase of one element must be at the expense of the other two; e.g., a brain tumor compresses and destroys brain tissue, causing displacement of CSF and blood. Displacement causes increased intracranial pressure (ICP), resulting in engorged venous return. Papilledema arises from increased venous pressure on the optic nerve head and retina

2. Note three key processes: a. Brain edema causes increased ICP. To compensate,

systemic BP is raised to maintain perfusion, and eventually the pulse drops. This is CUSHING’s TRIAD (increased BP, decreased HR, increased ICP), and heralds impending herniation

b. Brain herniation by mass lesions cause a shift of brain tissue from a compartment with high pressure to one with lower pressure. The three most common herniations are: i. Cerebellar tonsils into foramen magnum—posterior

fossa mass ii. Temporal lobe through the tentorium into the

posterior fossa iii. Medial/frontal or parietal lobes (central herniation)

under the falx into the opposite hemisphere. May not have focal neuro signs. +Cheyne-Stokes

iv. All cause varying LOC, focal neuro deficits/vomiting/HA, but the most important herniation involves the temporal lobe (usually the uncus) with clinical manifestations of rapid LOC, ptosis, ophthalmoplegia, hemiplegia ipsilateral to herniation, fixed pupil

Notes


D. Obstructive hydrocephalus

1. Presentation

a. Patients may have subtle complaints (mild headache) to dramatic presentations (full blown seizures, sudden death)

b. Changes in mental function: irritability, decreased memory, etc.

c. Headache: An early symptom in one-third of patients with tumors, but do not have a characteristic nature i. Dull and intermittent ii. Worse upon awakening

d. Vomiting: common e. Seizures: focal or generalized seizures in up to 20-50% of

patients with tumors i. NOTE: Focal neurologic deficits are uncommon.

Papilledema may be absent, but always check for it. Rarely, hearing loss or facial nerve palsy are due to pontine-cerebellar angle tumors

2. Diagnosis a. CT with contrast (uninfused scan shows only hemorrhage

or shift from tumor); MRI with gadolinium. b. Metastasis from a primary non-brain tumor is

common: look for possible primary sites (lung, breast, prostate).

c. After metastatic tumors, the most common primary brain tumors are gliomas (about 50%), meningiomas, et al.

3. Management a. ABCs, especially if presenting in coma, seizures. Airway

management must minimize increasing ICP i. Neurosurgical consultation early ii. May require high dose steroid (e.g., Decadron) to

decrease edema surrounding tumor iii. Controlled ventilation iv. Prophylactic anticonvulsants

IV. DISORDERS OF NERVE/MUSCLE

A. A variety of diseases with often vague presentation and complaints. These patients can be extremely difficult to diagnose in the emergency setting, but an awareness of the following disorders is important

B. Multiple sclerosis – An extremely difficult diagnosis to make in the

emergency department, but some points to remember: Pathologic hallmark: multifocal areas of demyelination and sclerosis at any level of the CNS. Generally thought to be an autoimmune disease.

Notes


More common in females, average age of onset 3rd to 4th decade

1. Clinically - see CNS lesions separated by time and space a. Visual b. Diplopia and oscillopsia c. Optic neuritis (loss of vision, usually central, with pain on

eye movement, see “washed out” colors, APD) d. Internuclear ophthalmoplegia (dysconjugate gaze when

looking laterally) e. Paresis of medial rectus (thought to be caused by

demyelination of medial longitudinal fasciculus) f. Cerebellar dysfunction: gait disturbance; spasticity; ataxia g. Weakness and/or numbness of extremities (lower > upper)

or face, hyperreflexia, clonus h. Sphincter disturbance: frequency, urgency, or incontinence i. Lhermitte’s phenomenon: tingling shock-like sensation

down the back and extremities with active or passive neck flexion

j. Rarely, see facial pain mimicking trigeminal neuralgia 2. Diagnosis

a. Is difficult, as any focal neurologic deficit can be caused by MS. i. MRI visualizes multiple areas of demyelination ii. Also used: visual evoked response (VER),

somatosensory evoked response (SER), and brainstem auditory evoked response (BAER)

iii. See oligoclonal bands or myelin basic protein in CSF. Note that CSF findings are not always conclusive, but about 95% of MS patients have one or more CSF abnormalities

3. Treatment a. Acute exacerbations: high dose IV Solu-Medrol (250-

500mg q12h) b. Optic neuritis: Solu-Medrol vs. Prednisone c. Suppression: Interferon B, Glatiramer, Estriol

4. Emergency presentations a. May include any of the above-mentioned clinical

complaints. Try to get a thorough history of any previous neurologic deficit in anyone presenting with a symptom suggestive of MS. Neurologic consultation

b. Patients with known diagnosis of MS may present with exacerbations, as well as infections (urinary, e.g.). Hot weather, hot baths, or concurrent infections cause elevated body temperature, which in turn may cause exacerbations

C. Myasthenia gravis

1. Symptomatic muscle weakness

Notes


2. Results from decreased number of acetylcholine receptors AChR) in the postsynaptic membrane, due to anti-AChR autoantibodies

3. Predilection for younger females (teens to early thirties) 4. Thymomas thought to cause increased AChR antibodies 5. Clinically

a. Acute or gradual onset of ptosis, dysphagia, slurred speech. Affects ocular, facial, pharyngeal, masticatory, and neck muscles. All symptoms demonstrate FATIGABILITY: worsening with movement and along the course of the day

b. Check for diplopia. Tell patient to repeatedly count aloud to precipitate slurred speech

c. Can see the “myasthenia snarl” from paralysis of facial and pharyngeal muscles; can lead to choking or aspiration

d. Be aware of MYASTHENIC CRISIS: an exacerbation severe enough to cause life-threatening respiratory failure

e. Diagnosis by history and physical, and measurement of serum acetylcholine receptor antibodies (positive in about 85% of patients with active MG)

f. EDROPHONIUM (TENSILON) test. Administer this short-acting anticholinesterase IV, and see improvement in muscle strength in about 1 minute and lasting for up to 5 minutes

g. Decremental response on EMG h. Be aware of CHOLINERGIC CRISIS in patients with

history of MG and treated with anticholinesterase inhibitor. Overmedication can lead to muscle weakness and mimic a myasthenic crisis

i. Also check for thymoma on CXR, or better, CT of chest j. Differential diagnosis to consider: Eaton-Lambert

syndrome, caused by certain malignancies but causes increased muscle strength with use; Botulism, caused by ingestion of Clostridium botulinum toxin, can cause diplopia, blurred vision, but see an incremental pattern on EMG

6. Treatment a. Primarily begins with an anticholinesterase, commonly

Pyridostigmine (Mestinon). Also used are steroids or immunosuppressives Occasional IVIG or plasma exchange

b. Thymectomy is recommended in most patients, especially those with thymomas

c. Watch for drugs that worsen MG by being weak neuromuscular blockers i. Many antibiotics, e.g., aminoglycosides, are to be

avoided. Check for this interaction before beginning any MG patient on new medication.

Notes


ii. Caution using NMBs for intubation D. Bell’s Palsy

1. Patients presenting with this facial nerve palsy often believe

they are having a CVA. Cause is not clear, but possibly HSV inflammation of the facial nerve. VSV causes Ramsey-Hunt syndrome with addition of vesicles around ear and neck

2. Clinically a. See weakness of ipsilateral facial muscles INCLUDING

THE FOREHEAD (peripheral lesion) b. Cannot close ipsilateral eye c. May see loss or distortion of taste d. 80-90% of patients recover (worse with Ramsay Hunt);

typically evolves over 1-3 days; about 10% will be left with permanent weakness or contracture

3. Treatment is generally supportive a. Patch affected eye (especially at night; artificial tears) b. Facial exercise c. Prednisone may help to relieve pain and/or prevent

chronic autonomic dysfunction; start 60 mg daily for 5-7 days, and taper over next week. Best if started in first 24 hours, but can be started within 1 week

d. Some authorities advise adding antiviral treatment in addition to Prednisone early in the clinical course (acyclovir or analogs). Studies support herpes simplex virus as etiology for Bell’s. Same treatment window as prednisone.

E. Guillain-Barré

1. An acute demyelinating polyneuropathy -- a symptom complex caused by infections, toxins, or collagen vascular disorders. Takes days or weeks to develop. May progress to respiratory failure

2. Clinically: see ascending weakness (bulbar involvement may be partial or total). Sometimes see sensory disturbances or pain. May have autonomic instability. Key feature on exam: LOSS of reflexes

3. Diagnosis: difficult a. Suspect if history of preceding infection or toxic-

metabolic insult, areflexia, and weakness b. Lumbar puncture shows normal CSF count and elevated

protein c. Nerve conduction studies, if done early, show conduction

block 4. DDX

a. Botulism

Notes


b. Diphtheria c. Myasthenia gravis d. Cord compression

5. Treatment a. Supportive: ventilatory support if needed b. Steroids generally not helpful c. Plasmapheresis vs. IVIG sometimes useful

V. NERVE COMPRESSION SYNDROMES

A. Spinal cord compression

1. From trauma, tumors, herniated disks, infections. Look for weakness in extremities, loss of sphincter tone, and areflexia. Diagnosis by either MRI or myelogram. Emergency decompression/steroids/ radiation usually indicated. Prompt consultation with neurosurgeon; early treatment

B. Common peripheral nerve disorders

1. L5 radiculopathy

a. Weak ankle eversion and inversion, ankle dorsiflexion, pain radiating to great toe

2. S1 radiculopathy a. Pain radiating from gluteal area down to lateral side of foot,

diminished ankle jerk, weak plantar flexion of ankle

C. Cauda equina syndrome

1. Injury to L/S/Coccygeal nerve roots 2. Etiology:

a. Ruptured disc b. Trauma c. Tumor d. Abscess

3. Symptoms: a. Motor/sensory loss in lower extremities b. Incontinence/retention of bowel/bladder c. “Saddle anesthesia” d. Can be unilateral

4. Treatment: a. Emergent surgical decompression b. Steroids (30 mg/kg IV bolus; 5.4 mg/kg/h IV over 24

hours) if traumatic

Notes


VI. AMYOTROPHIC LATERAL SCLEROSIS

A. Pathophysiology

1. Atrophy due to degeneration of neurons in anterior spinal cord and motor nuclei of lower brainstem; also atrophy of cells in motor cortex

B. Presentation

1. Affects men more commonly 2. Age of onset usually after 50 3. There are no particular typical presentations; symptoms usually

begin with subtle findings of clumsiness, awkward fine finger movements, and stiff fingers. Later, see fasciculations of upper body muscles. Other findings: a. Generalized hyperreflexia b. Slight spasticity of legs c. Atrophy of hands, forearms d. Numbness without objective sensory changes e. Involvement of neck, tongue, pharynx, larynx

C. Diagnosis

1. No specific emergency department testing 2. Some suggest EMG and nerve conduction studies

D. Treatment

1. Progresses over period of 1-5 years. 2. Respiratory compromise and aspiration are major risks for

morbidity; nebs, steroids, abx, intubation to maximize pulmonary function.

VII. TRIGEMINAL NEURALGIA (SEE HEADACHE SECTION) VIII. MASQUERADERS OF NEUROLOGIC DISEASE

A. Dementia

1. Chronic Alzheimer’s dementia patients can present to the emergency department due to anxiety or concern of family about deterioration

2. These patients can appear stuporous due to overmedication of sedatives ,e.g., Haldol

Notes


E. Drugs

1. Any drug that affects the CNS can lead to a change in mental

status, or lead to transient neurologic deficits. Common agents include sedative/anxiolytics (Haldol, benzodiazepines) in the elderly population. Street drugs are notorious for altered mental status: a. Cocaine b. Narcotics: patients can appear comatose c. PCP: acute agitation or confusion d. Psychedelics: confusion e. The list of street drugs in extensive. Remember the TOX

SCREEN in patients with neurologic presentations. (Bear in mind that “China White”, fentanyl, does not show up on standard drug screens; nor does “Ice”, an amphetamine or “Ecstasy”).

F. Parkinson’s disease

1. Patients can look stuporous, with motor stiffness. May present

with confusion state due to their anticholinergic or dopaminergic drugs.

Notes


NEUROLOGICAL EMERGENCIES

PEARLS

1. Treat headache in stepwise fashion. 2. New or changing character of headache requires work-up. 3. Look for autonomic symptoms for cluster headaches. 4. Get ESR in elderly patients with new headaches (for temporal arteritis). 5. Encephalitis can present with mental status change ONLY. 6. AIDS patients with ring-enhancing lesions on CT have toxoplasmosis until proven otherwise. 7. Start antibiotics on suspected meningitis cases before head CT. 8. Patients with sinus, ear infections are at higher risk for brain abscess. 9. Temporal lobe herniation can present with dilated ipsilateral pupil, ptosis, and stupor/coma. 10. Optic neuritis may be the herald sign of multiple sclerosis. 11. Ptosis and diplopia may be initial sign of myasthenia gravis. 12. Patients with Guillain-Barre are hyporeflexic. 13. Cauda equina is a neurosurgical emergency. 14. Bell's palsy patients lose ipsilateral forehead strength. 15. Pain in trigeminal neuralgia is spasmodic, not constant. 16. Get a tox screen in patients with acute mental status change.

Notes


REFERENCES 1. Tintinalli JE. Emergency Medicine: Comprehensive Study Guide. 6th Ed. New York: McGraw-Hill; 2004.

2. Marx JA, et al. Rosen’s Emergency Medicine Concepts and Clinical Practice. 5th Ed. St. Louis, MO: Mosby; 2002. 3. Goetz CG. Textbook of Clinical Neurology. 2nd ed. St. Louis, MO: Elsevier; 2003. 4. Goadsby P. J., Lipton R. B., Ferrari M. D. Drug Therapy: Migraine — Current Understanding and Treatment. N Engl J Med 2002; 346:257-270. 5. Ahn UM, Ahn NU, Buchowski JM et al. Cauda Equina Syndrome Secondary to Lumbar Disc Herniation: A Meta-Analysis of Surgical Outcomes. Spine 2000;25:1515–1522. 6. Clinical Policy: Critical Issues in the Evaluation and Management of Patients Presenting to the Emergency Department with Acute Headache. Ann Emerg Med 2002;39:108-122. 7. De Gans J, Van de Beek D. Dexamethasone in adults with bacterial meningitis. N Eng J Med. Nov 2002;347:1549-1556. 8/10

Documents

Neurological Emergencies · CVA e. Complex/complicated migraine/migrainous infarction i. Aura lasting 7 days ii. Can show infarction by MR/CT 4. Treatment: Abortive therapies; What