BASICS
Unilateral (sometimes bilateral) motor dysfunction of cranial nerve (CN) VII
ETIOLOGY
Associated with pregnancy, diabetes mellitus, trauma, infection, neoplasm, Lyme disease, herpes simplex virus
SIGNS AND SYMPTOMS
Abrupt onset of symptoms
Unilateral face paralysis of forehead and lower face
• Cannot close eye, raise eyebrow, smile on affected side
• Central lesions (i.e., stroke) spare the forehead
May include pain in ipsilateral ear, hyperacusis, impaired taste, lacrimation
DIAGNOSTICS
Clinical exam finding
Consider head CT or MRI if risk factors for CVA or symptoms atypical
TREATMENT
Most resolve spontaneously
Treat with oral prednisone
Consider acyclovir
Transection (Segmental) Syndrome
Loss of all sensation, weakness below affected level
Bladder dysfunction
Trauma, hemorrhage, abscess, transverse myelitis, metastatic lesions
Bilateral symptoms, including corticospinal tracts, central autonomic tracts to bladder
Gait ataxia, weakness, muscle flaccidity hyperreflexia
Ventral two-third of spinal cord, includes corticospinal tracts, spinothalamic tracts, descending autonomic tracts to bladder control
Muscle weakness and reflex changes, urinary incontinence
Focal to level of injury, do not ascend or descend
Loss of pain and temperature
Syringomyelia, tumor
Aka hemi cord
Lateral hemisection injury (trauma, bullet, stabbing) that affects the ipsilateral part of your body
Weakness, loss of proprioception, pain, temperature, and vibration
Only weakness no sensory changes
Upper motor neuronal injury = hyperreflexia, extensor plantar responses
Lower motor neuron injury = muscle atrophy and fasciculations
Chronic myelopathies
Lesions at L2
Early and significant urine/bowel incontinence
Saddle anesthesia (S3 to S5)
Tumors, disc herniation, fracture
BASICS
Chronic and progressive decline of function that interferes with independence and daily function
Nonreversible
Alzheimer disease is most common
ETIOLOGY
Reduced cerebral production of choline acetyl transferase, which leads to a decrease in acetylcholine synthesis and impaired function
SIGNS AND SYMPTOMS
Impairment in learning, reasoning, memory, handling complex tasks, spatial ability and orientation, language, learning and retaining new information
Aphasia, apraxia, agnosia, impaired executive function
DIAGNOSTICS
History and physical exam
History from family members is particularly beneficial
Screening for B12 deficiency and thyroid disorders
Cognitive testing
Mini-mental status exam
Structural imaging with MRI or CT to rule out other etiologies
TREATMENT
Symptomatic: treatment of behavioral disturbances, environmental manipulations to support function, and counseling
Cholinesterase inhibitors, such as tacrine, rivastigmine, galantamine
Memantine for moderate to severe Alzheimer dementia
BASICS
Acute, rapid, transient disturbance of consciousness
ETIOLOGY
Fluid and electrolyte disorders, infections, drug or alcohol toxicity or withdrawal, metabolic disorders, low perfusion states, postoperative states
SIGNS AND SYMPTOMS
Decreased ability to focus and change in level of awareness
Sleep impairment, hallucinations, distractible
Emotional disturbances, such as fear, depression, euphoria
DIAGNOSIS
History and physical exam, mental status exam
Lab testing and imaging to identify underlying etiology
TREATMENT
Correct underlying medical disorder
Antipsychotics for impulsive, violent, or unpredictable patients
BASICS
Acute immune-mediated polyneuropathy, progressing over about 2 weeks
ETIOLOGY
Exact cause is unknown
Sixty percent caused by a preceding infection
SIGNS AND SYMPTOMS
Progressive, symmetric muscle weakness, usually ascending
Weakness can be mild to nearly complete paralysis of all extremities, facial, respiratory, and bulbar muscles
Decreased DTRs, respiratory muscle weakness and depression, back and extremity pain, paresthesias
DIAGNOSIS
Cerebrospinal fluid from lumbar puncture (LP) reveals elevated protein with normal WBC
Electromyography and nerve conduction studies
TREATMENT
Plasmapheresis
IV immunoglobulin
Subdural, epidural, subarachnoid
• See specific section
Infections (meningitis, encephalitis, brain abscess)
• See specific section
Vascular:
• Malignant hypertension (HTN), vertebral dissection (associated with exertion, chiropractor), thrombosis, cerebral aneurysm
Temporal arteritis:
• Unilateral frontotemporal severe headache (HA), tender to palpation of temporal artery
• Diagnosis: erythrocyte sedimentation rate >50
• Treatment: prednisone
Age >50, rapid onset, severe intensity, no prior HA, fever, trauma, vision changes, immunosuppression, HTN, neuro deficits, altered mental status (AMS)
Tension
• Band-like, aching (nonpulsatile), bilateral, lacking secondary symptoms (nausea, vomiting, photophobia)
• No focal neuro deficits
• Tenderness to posterior cervical and temporal muscles
• Precipitated by stress, sleep deprivation, hunger, eyestrain, alcohol
• Treatment: supportive, nonsteroidal anti-inflammatory drugs, Tylenol, muscle relaxants
Cluster
• Severe, burning/pulsating, unilateral, periorbital HA with associated ipsilateral lacrimation, conjunctival injection, nasal congestion, myosis, ptosis
• Short duration occurring several times per day for weeks
• Most commonly in male >30 years
• Treatment: high-flow O2, IM/intranasal triptans
Migraine
• Unilateral, severe, throbbing, associated photophobia, phonophobia, nausea, vomiting, aura (visual, auditory, smell)
• Common in women near menses, family history
• Treat with analgesia/antiemetics (Tylenol, nonsteroidal anti-inflammatory drugs, chlorpromazine, Reglan)
Adjust environment (quiet/dark room)
Caffeine
Triptans
Ergotamines (do not use ergotamine within 24 hours of triptan use due to vasoconstrictive effect)
• Prophylaxis propanolol, amitriptyline, fluoxetine, Topamax, Neurontin, valproate
BASICS
Autoimmune neuro muscular disorder characterized by muscle weakness
ETIOLOGY
Antibodies block acetylcholine receptor in the postsynaptic membrane
Onset in the second and third decades (females predominantly) or sixth to eighth decade (males)
SIGNS AND SYMPTOMS
Features fluctuating muscle weakness and fatigue, tends to be worse later in the day and with repetitive activity
Diplopia, ptosis, dysarthria, dysphagia, loss of facial muscles, “loss of smile”
Respiratory muscle weakness is most serious, can cause respiratory failure, or “myasthenic crisis”
DIAGNOSTICS
Clinical diagnosis by history and physical
Tensilon test: administering an anticholinesterase drug which will temporarily relieve muscle weakness
Serologic test for antibodies
Electromyography to detect impaired muscle to nerve transmission
CT or MRI to rule out thymoma (present in 10% to 15% of patients with MG)
TREATMENT
Symptom control by anticholinesterase drugs such as neostigmine or pyridostigmine
Steroids and immunosuppressive drugs such as prednisone and tacrolimus to suppress production of antibodies
BASICS
Damage to the peripheral nervous system
May affect sensation, movement, organ function
ETIOLOGY
Metabolic (diabetes, hypothyroid, liver failure)
Vitamin deficiency
Medication (chemotherapy)
Traumatic injury
Excessive alcohol consumption
Immune system disease or infection (Guillain–Barré, lupus, leprosy, multiple sclerosis, Lyme disease)
Shingles
SIGNS AND SYMPTOMS
Gradual onset of numbness and tingling in hands and feet
Burning, sharp, electric-like pain
Extreme sensitivity to touch and heat intolerance
Muscle weakness if motor nerves are affected
Ankle jerk reflex is classically absent in peripheral neuropathy
DIAGNOSTICS
History and physical, including neurologic exam
Lab testing: CT, MRI, LP to exclude other causes
Electromyography
TREATMENT
There is no cure
Depends on the cause and is focused on treating symptoms
Antiseizure medications, including Gabapentin (Figure 10.1)
SEIZURE AND STATUS EPILEPTICUS
BASICS
Partial:
• Simple
Consciousness preserved
Isolated limb jerking or “Jacksonian march”—motor symptoms that start in one part of body and march down the rest
FIGURE 10.1. Characteristic sensory disturbances found in various spinal cord lesions in comparison with peripheral neuropathy. (From Daroff RB, Fenichel GM, Jankovic J, Mazziotta JC, eds. Bradley’s Neurology in Clinical Practice. 6th ed. Philadelphia, PA: Saunders Elsevier; 2012. Figure 24.2 MD Consult.)
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