Nervous System
Acute Bacterial Meningitis
High-Risk Groups: Neonates, infants, and older patients face the highest risk for this life-threatening infection.
Common Pathogens (Community-Acquired):
Streptococcus pneumoniae (approximately 50\%)
Neisseria meningitidis (approximately 30\%)
In adults, also Haemophilus influenzae (gram-negative).
Classic Symptoms:
Acute onset of high fever (greater than \text{100.4}^{\circ}\text{F} or \text{38}^{\circ}\text{C})
Severe headache
Stiff neck (nuchal rigidity)
Altered mental status (confusion, lethargy, stupor)
Often meningococcal disease (refer to "Danger Signals" in Chapter 6)
Classic purple petechial rashes may appear.
Accompanied by nausea, vomiting, and photophobia.
Progression: Rapid worsening of symptoms progressing to lethargy, confusion, and finally coma.
Urgency: If not treated, it is fatal. Bacterial meningitis is a medical emergency; call \text{911}.
Reportable Disease: Bacterial meningitis is a reportable disease to the local health department.
Laboratory Tests & Diagnosis:
Initial Blood Work: Complete blood count (CBC) with differential, complete metabolic panel, coagulation studies, and blood cultures (\times\text{2}).
CT Scan (Pre-LP): Obtain a CT scan of the head before a lumbar puncture (LP) if the patient has any of the following risk factors: papilledema, focal neurologic deficit, abnormal level of consciousness (LOC), new-onset seizure (within 1 week of presentation), history of central nervous system (CNS) disease (stroke, mass), or immunocompromise (HIV, immunosuppressive therapy, solid organ or bone marrow transplant).
Lumbar Puncture (LP):
Elevated opening pressure.
Cerebrospinal fluid (CSF) contains large numbers of white blood cells (WBCs) and is cloudy.
Definitive diagnosis involves isolating bacteria from the CSF, with elevated protein and low glucose levels in the CSF.
Antimicrobial Therapy Timing: Do not delay antimicrobial therapy if LP is delayed by imaging studies. Obtain blood cultures and start empiric antibiotics as soon as possible.
Gram Stain & Culture: Gram stain and culture and sensitivity (C&S) of CSF and blood are needed to confirm diagnosis by isolating a bacterial pathogen.
Treatment Plan:
Antimicrobials (Adults): Third-generation intravenous (IV) cephalosporin (e.g., cefotaxime and ceftriaxone) PLUS vancomycin PLUS ampicillin (for adults >50 years).
Corticosteroids: Dexamethasone is recommended for adults with suspected bacterial meningitis in addition to antimicrobial therapy.
Supportive Care: Fluid management, reduction of intracranial pressure (ICP), and prevention of neurologic complications.
Complications:
Patients who recover often have some degree of permanent neurologic sequelae.
Older patients have a higher mortality rate due to comorbid conditions.
Acute Stroke (Cerebrovascular Accident)
Classification:
Ischemic (about 80\%)
Subtypes: thrombosis, embolism, and systemic hypoperfusion.
Hemorrhagic (about 20\%)
Ischemic Stroke Presentation:
Acute onset of stuttering/speech disturbance.
One-sided facial weakness.
One-sided weakness of the arms and/or legs (hemiparesis).
Patient may describe a "thunderclap-type" acute headache.
Hemorrhagic Stroke Presentation:
Often seen in patients with poorly controlled hypertension.
Abrupt onset of a severe headache, nausea/vomiting, and nuchal rigidity (suggestive of subarachnoid hemorrhage [SAH]).
Urgency: Call \text{911}.
Detailed Classification & Risk Factors:
Ischemia Causes: Emboli (cardiac, aortic, arterial, unknown source), thrombosis (large or small vessel disease), or systemic hypoperfusion.
Hemorrhage Types: Intracerebral (bleed directly into the brain) and subarachnoid (bleeding into subarachnoid space and CSF).
Impact: Obstruction or bleeding causes permanent brain damage.
Modifiable Ischemic Stroke Risk Factors: Hypertension, dyslipidemia, diabetes, smoking, physical inactivity.
Hemorrhagic Stroke Risk Factors: Older age, hypertension, cigarette smoking, family history, alcohol use, sympathomimetic drug use, antithrombotic therapy (antiplatelet and anticoagulant).
Cause of Most SAHs: Rupture of intracranial aneurysms.
Demographic Disparities: Black and Hispanic Americans have increased stroke risk compared with White Americans.
"Stroke Belt": Refers to the southeastern United States, an area with a higher regional incidence, prevalence, and mortality rate of strokes.
Classic Case (Embolic Stroke): Abrupt onset of difficulty speaking, unilateral hemiparesis, and weakness of the arms or legs (or both).
Classic Case (Hemorrhagic Stroke): Initially presents with severe headache, nausea/vomiting, photophobia, nuchal rigidity, accompanied by hemiparesis and difficulty speaking.
Specific Hemorrhagic Stroke Features:
SAH:
Sudden onset of severe "thunderclap headache" described as "the worst headache of my life."
Pain may radiate and cause neck pain or stiffness (meningismus).
May or may not be associated with a rapid decrease in or loss of consciousness (coma, death), seizures, nausea, vomiting, and/or focal neurologic deficit.
Usually begins abruptly compared to more gradual intracranial hemorrhage (ICH).
Sentinel Headache: A sudden and severe headache that may precede a major SAH by days to weeks prior to aneurysm rupture.
ICH:
Signs and symptoms vary by location and size, often gradual and progressing over minutes to hours.
Clinical presentation includes acute onset of focal neurologic deficit (hemiparesis, aphasia, visual impairment).
Large hemorrhages may cause headache, vomiting, and decreased LOC.
Precipitating Factors: Hemorrhagic stroke may be precipitated by sex or other physical activity.
Acute Ischemic Stroke Signs & Symptoms:
Dependent on the affected brain region.
May include sudden, severe headache, abrupt onset of hemiparesis, visual field deficits, facial droop, ataxia, nystagmus, aphasia, sudden numbness or weakness of face/extremity, abrupt decrease in LOC.
Middle cerebral artery is the largest and most commonly affected.
Left Middle Cerebral Artery Occlusion (Superior Branch): Right-sided facial weakness, right arm/leg weakness, hemianopia, expressive aphasia (Broca's area).
Right Middle Cerebral Artery Occlusion: Left-sided facial weakness, left arm/leg weakness, hemineglect, possible hemianopia.
Embolic Strokes: Sudden onset; deficits indicate focal brain function loss. Can occur when getting up at night (e.g., to urinate, or with sudden coughing/sneezing).
Thrombotic Strokes: Progression fluctuates with periods of improvement. Patients may have a neck bruit.
Systemic Hypoperfusion: Reduced perfusion from cardiac pump failure or reduced cardiac output, leading to generalized hypoxemia and decreased oxygen-carrying capacity to the brain.
Treatment Plan (Pre-ED):
Call \text{911}.
Assess ABCs (airway, breathing, circulation) immediately: airway patency, chest movement, bilateral breath sounds, circulation.
Check and stabilize vital signs and assess neurologic status.
Emergency Department Management:
Assess ABCs and stabilize the patient.
Determine if ICH is present and if reperfusion therapy (IV thrombolysis or mechanical thrombectomy) is appropriate for ischemic stroke.
Initial Imaging: Non-contrast CT scan of the head, then MRI if indicated.
Time Sensitivity: IV thrombolytic therapy with alteplase improves outcomes for acute ischemic stroke with symptom onset \le\text{4.5} hours.
Monitoring: Cardiac monitoring for at least the first 24 hours.
Lab Tests: CBC, coagulation panel, serum electrolytes and creatinine, fasting blood glucose, lipid panel, hemoglobin A1C, ESR, and CRP.
Hemorrhagic Stroke Evaluation: Evaluate for bleeding disorder.
Complications of Stroke:
Cardiac: Myocardial infarction (MI), arrhythmias, neurogenic cardiac damage.
Psychiatric: Depression, fatigue.
Dysphagia: Risk factor for aspiration pneumonia.
Physical: Falls and bone fractures.
Infection: Pneumonia, urinary tract infection.
Neurologic:
Apraxia (difficulty performing purposeful movements).
Broca's aphasia ("expressive aphasia"): Patient comprehends speech well but has difficulty with motor aspects of speech (speech length usually less than four words). Localized to frontal lobe lesions.
Wernicke's aphasia ("receptive aphasia"): Difficulty with comprehension but no problem producing speech. Reading and writing impaired.
Intracranial complications: cerebral edema, symptomatic hemorrhagic transformation of ischemic stroke, elevated ICP, hydrocephalus.
Early neurologic deterioration and seizures.
Pulmonary: Neurogenic pulmonary edema, abnormal respiratory patterns, sleep-related breathing disorders.
Gastrointestinal: Bleeding.
Urinary: Incontinence.
Vascular: Venous thromboembolism and pulmonary embolism.
Long-Term Management:
Blood pressure (BP) management.
Cholesterol management with low-density lipoprotein cholesterol (LDL-C)–lowering therapy.
Ischemic Strokes: Antithrombotic therapy.
Hemorrhagic Strokes: Discussion of risks/benefits of antiplatelet therapy and anticoagulation.
Glycemic control for diabetes patients.
Lifestyle and dietary changes.
Rehabilitation (physical, occupational, speech therapy).
Follow-up imaging as clinically indicated.
Chronic Subdural Hematoma (SDH)
Definition: Bleeding between the dura and subarachnoid membranes of the brain.
Presentation: Presents gradually, with symptoms potentially not appearing until weeks after the injury.
Patient History: History of head trauma (e.g., falls, accidents).
Symptoms: Headaches and gradual cognitive impairment (apathy, somnolence, confusion).
Increased Risk Factors: Alcohol use disorder, older adults, and those on anticoagulation or aspirin therapy.
Dangerous Headaches
Key Characteristics:
Thunderclap headache: Very severe, reaches maximum intensity in 1 minute or less.
"Worst headache of my life."
First onset of headache at age \ge\text{50} years.
Sudden onset after coughing, exertion, straining, or sex (exertional headache).
Sudden change in level of consciousness (LOC).
Focal neurologic signs: Unequal pupil size, hemiparesis, loss of function, poor gag reflex, difficulty swallowing, aphasia, sudden vision loss, visual field defect.
Headache with papilledema (increased intracranial pressure [ICP]).
"Worst-Case" Scenarios to Rule Out:
SAH or acute subdural hemorrhage.
Leaking aneurysm or arteriovenous malformation (AVM).
Bacterial meningitis.
Increased ICP.
Brain abscess.
Brain tumor.
Giant Cell Arteritis (GCA) / Temporal Arteritis
Overview: Also known as Horton disease, cranial arteritis, or temporal arteritis. A systemic inflammatory disorder (vasculitis) of the medium and large arteries.
Key Consideration: Should be considered in any patient over 50 years old with:
New headache or change in preexisting headache.
Abrupt visual disturbances or vision loss.
Jaw claudication.
Unexplained fever.
Signs/symptoms of vascular abnormalities.
Pain Description: Some patients experience excruciating burning pain over the affected temporal artery instead of a headache.
Physical Exam Findings: The affected temple has an indurated, reddened, and cord-like temporal artery that is tender and warm to the touch, accompanied by scalp tenderness.
Peak Incidence: Between ages 70 and 79 years.
Associated Conditions: Polymyalgia rheumatica (PMR) is associated with GCA, occurring in about \text{40\%} to \text{50\%} of GCA patients.
Complications: If untreated, GCA can lead to permanent blindness (ischemic optic neuropathy).
Classic Case: Older male patient with a headache on his temple, marked scalp tenderness on the same side, and an indurated, cord-like, warm, and tender temporal artery. May have jaw claudication (pain with chewing relieved by stopping) and visual symptoms like amaurosis fugax (transient monocular vision loss or partial visual field defect) or blindness. Systemic symptoms like low-grade fever and fatigue can also be present.
Laboratory Findings:
Markedly elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are common but nonspecific for GCA.
Other labs: CBC, complete metabolic panel (creatinine, liver function tests, glucose), urine dipstick, serum protein electrophoresis, bone profile panel (calcium, phosphorus, albumin, total protein, alkaline phosphatase, 25-hydroxyvitamin D).
Treatment Plan:
Referral: Refer to ophthalmologist or rheumatologist, or to the ED stat.
Definitive Diagnosis: Temporal artery biopsy (outpatient, local anesthesia). Temporal artery color Doppler ultrasound is an alternative.
First-Line Treatment: High-dose systemic glucocorticoids (prednisone \text{40-60 mg PO} daily or methylprednisolone \text{500-1000 mg IV} daily) to preserve vision.
Subsequent Management: Glucocorticoid tapering, monitoring disease activity, imaging surveillance for large vessel involvement.
Tips/Pearls:
Initial treatment is with high-dose glucocorticoids for several weeks.
ESR and CRP are almost always elevated but are nonspecific.
Regard with high index of suspicion due to risk of blindness. Treat with oral steroids ASAP if suggestive history/exam, and/or refer to ED.
Serial labs (ESR, CRP) should be ordered until symptoms improve and monitored frequently.
Multiple Sclerosis (MS)
Overview: Autoimmune disease where antibodies attack the myelin sheath, causing demyelination.
Epidemiology:
Peak incidence: 15 to 45 years of age.
More common in women (\text{2.3:1}) and White people.
Affected Areas: Tends to affect the optic nerves (CN II), spinal cord, brainstem, cerebellum, and white matter.
Subtypes:
Relapsing-remitting MS (\text{85\%}–\text{90\%} of cases).
Primary progressive MS (\text{10\%}).
Secondary progressive MS.
Clinically isolated syndrome (precursor to MS).
Classic Case: Adult female patient complains of episodic visual loss or diplopia (double vision), problems with balance and walking, numbness and paresthesia on one side of the face.
Accompanied by urinary incontinence (\text{75\%}) and/or bowel dysfunction (\text{50\%}).
Reports Lhermitte sign: Electric shock-like sensation running down the back when bending neck forward/flexion.
Urgency: Not emergent, but recognition of signs/symptoms is crucial for diagnosis and treatment.
Diagnosis:
Primarily clinical based on history and physical examination.
Imaging: MRI of brain and spinal cord is the test of choice to assess for MS lesions.
CSF Analysis: Assess for oligoclonal bands and/or an increased immunoglobulin G index.
Treatment Plan: Refer to a neurologist for management.
Subarachnoid Hemorrhage (SAH)
Overview: Life-threatening condition.
Presentation:
Sudden and rapid onset of severe headache described as "the worst headache of my life."
Accompanied by nausea/vomiting.
Neck pain or stiffness (positive Brudzinski and/or Kernig signs).
Photophobia.
Visual changes (diplopia, visual loss).
Rapid decline in level of consciousness (LOC).
Headache Location: May be nonlocalized or localized in the occipital area and neck.
Seizures: May have seizures during the acute phase.
Vital Signs: Blood pressure (BP) elevation, temperature elevation, and tachycardia.
Neurologic Signs: Depending on the bleed source, focal neurologic signs may or may not be present.
Etiology: Usually caused by ruptured cerebral aneurysm or AVM.
"Sentinel Headache": A sudden intense headache that can precede a spontaneous SAH by days to weeks.
Diagnosis: Non-contrast CT scan can detect SAH in approximately \text{95\%} of patients within the first 24 hours.
Mortality: Associated with a high early mortality rate; some patients die suddenly before hospital evaluation.
Urgency: A medical emergency; call \text{911}.
Neurologic Exam
Components: Includes mental status, cranial nerves (CNs), and motor, reflex, and sensory examinations.
Folstein Mini-Mental State Exam (MMSE)
A detailed review is found in Chapter 16 "Psychiatric-Mental Health Review."
Cerebellar Testing
Function: The cerebellum coordinates unconscious regulation of balance, muscle tone, and voluntary movements.
Tests:
Gait:
Instruction: Walk to the other side of the room and back (with walking aid if used).
Observation: Shuffling, scissoring, waddling, or swinging gait.
Positive Finding: Acute cerebellar ataxia presents with a wide-based staggering gait.
Tandem Gait:
Instruction: Walk a straight line normally, then walk heel-to-toe.
Positive Finding: Inability to perform tandem walking, loss of balance, or falls.
Rapid Alternating Movements:
Instruction: Place hands on top of each thigh and rapidly alternate between supination and pronation.
Positive Finding: Inability to perform or problems with rapid alternating movements (dysdiadochokinesia).
Heel-to-Shin Testing:
Instruction (supine with extended legs): Place left heel on right knee, then move it down the shin (repeat with right heel on left knee).
Positive Finding: Inability to keep the foot on the shin.
Finger-to-Nose and Finger-to-Finger Test:
Instruction: Fully extend arm, touch nose, or touch nose then extend arm and touch examiner's finger.
Positive Finding: Inability to touch or missing the nose/finger (dysmetria).
Proprioception: Romberg Test
Instruction: Stand with arms/hands straight at sides, feet together, eyes open (observe). Then close eyes and maintain position (observe).
Positive Finding: Patient with eyes closed sways excessively, falls, or has to keep feet wide apart to maintain balance. Suggests cerebellar ataxia/dysfunction or sensory loss.
Cranial Nerve Testing
Mnemonic for Names: "On Old Olympus Towering Tops, A Finn And German Viewed Some Hops." (First letter corresponds to CN name and number).
Mnemonic for Function (Sensory, Motor, or Both): "Some Say Marry Money, But My Brother Says Big Brains Matter Most." (S=Sensory, M=Motor, B=Both).
Specific CNs:
CN I: Olfactory (On): Test with familiar scent (e.g., coffee, peppermint); block one nostril at a time.
CN II: Optic (Old):
Visual Field Testing: Patient \text{2} feet from examiner, cover one eye. Examiner stretches arm peripherally, asks patient to identify 1, 2, or 3 fingers (all 4 quadrants). Examiner serves as control.
Central Distance Vision: Snellen chart (\text{20} feet away).
CN III: Oculomotor (Olympus):
Usually tested with CN IV and CN VI (control extraocular muscles [EOM]).
Look for ptosis. Follow examiner's fingers (observe for nystagmus – horizontal quick eye movements alternating with slower opposite movements).
Test pupillary function.
CN IV: Trochlear (Towering): Controls down and inward eye movement. Tested with CN III and CN VI.
CN V: Trigeminal (Tops):
Muscles of mastication.
Sensory nerves to face, scalp, cornea, mucous membranes, nose.
Test sensation by lightly touching forehead (V1 ophthalmic), cheek (V2 maxillary), and chin (V3 mandibular) with eyes closed.
Tip: Herpes zoster infection (shingles) of CN V ophthalmic branch (V1) can lead to corneal blindness, especially if rash at tip of nose and temple.
CN VI: Abducens (A): Controls lateral eye movement. Tested with CN III and CN IV.
CN VII: Facial (Finn):
Controls facial muscles for expressions.
Instructions: Close eyelids tightly (try to open manually), look up and wrinkle forehead, smile.
Observe for asymmetry and muscle atrophy.
Bell's Palsy: Inflammation of the motor portion of CN VII; affected side of face will not move, eyelid may not fully close.
CN VIII: Acoustic (And): Hearing exam (rub hair in front of ear, whisper numbers, use hand as sound screen).
CN IX: Glossopharyngeal (German) & CN X: Vagus (Viewed):
Both control the palate; usually tested together.
Instruction: Open mouth and yawn (observe for asymmetry, uvula should be midline).
Gag reflex (lightly touch back of throat with tongue blade).
Assess voice clarity (rule out dysarthria).
CN X also involved in swallowing, sensation from carotid body, carotid reflex.
Tip: CN IX innervates movement of soft palate (ask patient to yawn or say "aah" to check voice clarity).
CN XI: Spinal Accessory (Some):
Controls shoulder shrug and head rotation.
Instructions: Shrug shoulders (should be level). Rotate head to left, push against examiner's hand on left cheek (repeat for right).
Check sternocleidomastoid muscle for atrophy or asymmetry.
Tip: The number \text{XI} reminds you of shoulders shrugging together.
CN XII: Hypoglossal (Hops): Controls tongue movement. Instruction: Stick out tongue and move it side to side. Look for atrophy and asymmetry.
Sensory System
Instruction: Patient closes eyes for all tests.
Tests:
Monofilament Testing: Randomly place monofilament on several sites of plantar and dorsal surfaces of each foot; apply pressure until filament bends.
Vibration Sense: Use 128\text{-Hz} tuning fork; tap, then place on distal joint of each thumb and tips of toes/soles of feet (compare feet). Check for numbness or decreased sense.
Importance: Important test for assessing severity of diabetic peripheral neuropathy.
Finding: Vibration sense is often the earliest to be affected in peripheral neuropathy (polyneuropathy), caused by diabetes and vitamin B12 deficiency anemia.
Sharp–Dull Touch: Use sharp (safety pin/toothpick) and dull (safety pin head/pencil eraser) ends.
Temperature: Test ability to differentiate hot/cold.
Positive Results: Inability to feel monofilament, discriminate sharp from dull, feel hot/cold, or sense vibration.
Stereognosis
Definition: Ability to recognize familiar objects through touch only.
Test: Place familiar object (coin, key, pen) on patient's palm, ask to identify with eyes closed.
Graphesthesia
Definition: Ability to identify figures "written" on skin.
Test: "Write" a large letter or number on patient's palm with fingers (patient's eyes closed).
Motor Exam
Upper Extremities: Raise both arms, pronate/supinate; bend/extend forearms, push against resistance.
Hands: Full range of motion with/without resistance. Dominant hand may be slightly larger.
Lower Extremities (Supine): Flex each hip, raise each leg separately against resistance; compare legs.
Feet: Full range of motion for toes and ankles; examiner provides resistance.
Pronator Drift Test:
Instruction: Stretch arms out palms up, eyes open; then close eyes for \text{20-30} seconds, tap arms briskly downward.
Positive Finding: One arm drifts downward.
Indicates: Upper motor neuron diseases (stroke, amyotrophic lateral sclerosis [ALS], polio).
Lower Motor Neuron Lesions: Look for muscle weakness, wasting/atrophy, fasciculations (e.g., neuropathy, polio, nerve root compression/radiculopathy).
Gross & Fine Motor Movements: Test walking, manipulation/pincer grasp, jumping.
Reflexes
Comparison: Both sides should be equal.
Spinal Nerves: 31 pairs of spinal nerve roots, each innervating distinct dermatomal distributions.
Grading Reflexes:
\text{0}: No response
\text{1+}: Low response
\text{2+}: Normal or average response
\text{3+}: Brisker than average response
\text{4+}: Very brisk response (sustained clonus)
Reflex Testing:
Quadriceps Reflex (Knee-Jerk): Reflex center L2 to L4. Tap patellar tendon briskly.
Achilles Reflex (Ankle-Jerk): Reflex center L5 to S2 (tibial nerve). Legs dangling, hold foot in slight dorsiflexion, briskly tap Achilles tendon.
Finding: Weak to no response with peripheral neuropathy (diabetes, vitamin B12 deficiency anemia).
Plantar Reflex (Babinski's Sign): Reflex center L4 to S2. Stroke plantar surface of foot on lateral border from heel toward big toe.
Normal Response (Adults): Plantar flexion (negative Babinski's).
Positive Finding (Adults): Toes spread like a fan. (Abnormal in adults, normal in young infants).
Pearl: Acute onset of cerebellar ataxia is a medical emergency; may indicate an acute vascular event. Requires neuroimaging and screening for causative drugs/toxins.
Deep Tendon Reflexes by Nerve Root:
Biceps & Brachioradialis: C5-6
Triceps: C6-7
Hip flexion/extension: L2-3 / L4-5
Knee extension (knee jerk)/Knee flexion: L3-4 / L5-S1
Achilles (ankle jerk): S1
Neurologic Maneuvers (Meningeal Irritation)
Purpose: Assess for meningeal irritation (suggestive of meningitis or SAH).
Patient Position: All done with patient supine.
Sensitivity: More sensitive in children than adults.
Tests:
Kernig's Sign:
Instruction: Flex hips one at a time, then attempt to straighten the leg while keeping hip flexed at \text{90} degrees.
Positive Finding: Resistance to leg straightening due to painful hamstrings (inflammation on lumbar nerve roots) and/or complaints of back pain.
Brudzinski's Sign:
Instruction: Passively flex/bend patient's neck toward the chest.
Positive Finding: Patient reflexively flexes hips and knees to relieve pressure and pain (inflammation of lumbar nerve roots).
Nuchal Rigidity:
Instruction: Touch chest with the chin.
Positive Finding: Inability to touch the chest secondary to pain.
Acute Mild Traumatic Brain Injury (Concussion)
Early Symptoms: Confusion, headache, dizziness/vertigo, poor balance, nausea/vomiting.
Consciousness: Most do not lose consciousness.
Amnesia: Antegrade and retrograde amnesia are common after injury.
Definition: Glasgow Coma Scale (GCS) score of \text{13} to \text{15} (measured 30 minutes after injury).
Epidemiology: Most patients are male (\text{2:1}).
Mechanism: Usually results from acceleration/deceleration forces on brain tissue.
Common Causes: Motor vehicle collisions, falls, occupational accidents, recreational accidents, assaults. Sports with highest rates: American football, ice hockey, soccer, boxing, rugby. Common wartime injury for soldiers in combat.
Treatment Plan:
History: Ask about accident details (events leading up to, during, and after concussion).
Medication History: Inquire about anticoagulation, chronic acetylsalicylic acid (ASA) therapy, or nonsteroidal anti-inflammatory drugs (NSAIDs) due to higher risk of brain hemorrhage.
Assessment: Evaluate mental status (short-term memory, attention), perform neurologic assessment and CN examination (focus on vision CN II, pupil exam, EOM CN III, IV, VI, facial movements CN VII).
Referral: Refer to ED if suspected head trauma; may need a CT scan of head (without contrast).
Indications for Hospital Admission:
GCS score <\text{15}
Seizures or other neurologic deficit(s)
Recurrent vomiting
Abnormal head CT (e.g., midline shift, hemorrhage, ischemia, mass effect)
Abnormal bleeding
Bell's Palsy
Definition: Abrupt onset of unilateral facial paralysis due to dysfunction of the motor branch of the facial nerve (CN VII).
Progression: Facial paralysis can progress rapidly within 24 hours.
Sensation: Skin sensation remains intact.
Tear Production: Tear production on the affected side may stop.
Resolution: Most cases resolve spontaneously.
Suspected Cause: Herpes simplex virus activation.
Classic Case: Older adult wakes up with one side of face paralyzed. Reports difficulty chewing/swallowing on same side. Unable to fully close eyelid on affected side.
Treatment Plan:
Early Glucocorticoids: High-dose oral glucocorticoids (prednisone \text{60-80 mg/day}) for 1 week, started within 3 days of onset.
Antivirals (Severe Palsy): Coadministration of antiviral therapy (valacyclovir \text{1,000 mg} TID OR acyclovir \text{400 mg} five times daily) imes\text{7} days.
Corneal Protection: Apply artificial tears (liquid, gel) every hour while awake, use protective glasses/goggles. At night, use ointment (mineral oil, white petrolatum) and eye patch.
Complications: Can cause corneal ulceration. Recurrent attacks in \text{7\%} to \text{15\%} of cases.
Carpal Tunnel Syndrome (CTS)
Definition: Compression of the median nerve as it travels through the carpal tunnel.
Causes: Commonly caused by activities requiring repetitive wrist/hand motion.
Bilateral Involvement: Both hands affected in \text{50\%} of patients.
Risk Factors: Genetic predisposition, diabetes mellitus, thyroid disease, pregnancy, osteoarthritis, rheumatoid arthritis, wrist trauma, obesity.
Epidemiology: More common in women (\text{3:1}).
Classic Case: Adult female with gradual onset (weeks to months) of numbness and tingling (paresthesia) in median nerve territory (thumb, index finger, middle finger).
Weaker hand grip on affected hand.
Difficulty lifting heavy objects.
Symptoms worse with repetitive hand/wrist actions and at night (awakens patient).
Chronic severe cases show thenar eminence atrophy (late sign).
History of occupation/hobby with frequent wrist/hand movements.
Diagnostic Signs:
Tinel's Sign:
Purpose: Identify nerve compression.
Test (Median Nerve): Tap over the anterior wrist (carpal tunnel).
Positive: "Pins and needles" or tingling in median nerve distribution (thumb, index, middle fingers).
Test (Ulnar Nerve): Tap over cubital tunnel at elbow to elicit symptoms in ring and little fingers.
Phalen's Sign:
Purpose: Identifies median nerve pathology.
Test: Full flexion of wrist for \text{60} seconds.
Positive: Numbness or tingling sensation of the median nerve over the hand evoked by passive flexion.
Tips: Recognize Tinel's and Phalen's signs for CTS (median nerve compression). CTS refers to signs/symptoms from median nerve compression.
Screening for Visual Field Loss
Homonymous Hemianopia: Visual field loss involving either the two left halves or the two right halves of the visual field. Most common cause is stroke.
Screening Test: Visual fields by confrontation.
Headaches: Classic Signs and Symptoms
Migraine without Aura
Symptoms: Throbbing pain behind one eye, photophobia, phonophobia, nausea/vomiting.
At-Risk: Adult females.
Aggravating Factors: Stress, menstruation, visual stimuli, weather changes, nitrates, fasting, wine, sleep disturbances, aspartame.
Migraine with Aura
Symptoms: Preceding symptoms (visual scotoma, scintillating lights, halos, tingling down one limb, dysphasia, motor weakness [hemiplegic migraine]) followed by migraine headache.
At-Risk: Adult females.
Aggravating Factors: Stress, menstruation, visual stimuli, weather changes, nitrates, fasting, wine, sleep disturbances, aspartame.
Trigeminal Neuralgia
Symptoms: Intense, very brief, sudden, usually unilateral sharp stabbing pain in one or more branches of CN V.
At-Risk: Older adults and elderly.
Aggravating Factors: Cold food, cold air, talking, touch, chewing.
Cluster Headache
Symptoms: Severe "ice-pick" piercing pain behind one eye, with tearing, eye redness, rhinorrhea, ptosis, and miosis on one side (Horner's syndrome).
At-Risk: Middle-aged males.
Aggravating Factors: Occurs at same time daily in clusters for weeks to months (usually at night); alcohol consumption.
Giant Cell Arteritis
Symptoms: Unilateral pain (temporal area) with scalp tenderness; skin over artery is indurated, tender, warm, and reddened; amaurosis fugax (temporary blindness) may occur.
At-Risk: Older adults and elderly.
Aggravating Factors: Various genetic and environmental factors.
Tension Type Headache
Symptoms: Bilateral "band-like" pain, vise-like or tight quality, continuous dull pain (usually generalized), may last several hours; may be accompanied by spasms of trapezius muscles.
At-Risk: Adults.
Aggravating Factors: Emotional or physical stress and mental tension, head and neck movements.
Medication Overuse Headache (Rebound Headache)
Definition: Headache occurring \ge\text{15} days per month due to overuse of acute headache medications for >3 months.
Epidemiology: More common in women, patients with migraine who are depressed or anxious.
Symptoms: Daily or almost-daily headaches, accompanied by irritability, depression, insomnia.
Causes: Overuse of abortive medicines (analgesics, NSAIDs, aspirin, combination NSAID/acetaminophen with caffeine, butalbital, barbiturates, ergots, triptans, opioids).
Highest risk with opioids, butalbital-containing combination analgesics, and acetaminophen-aspirin-caffeine combinations.
Treatment:
Discontinue medication immediately (if not contraindicated) or gradually taper dose/reduce frequency.
Bridge therapy (e.g., NSAIDs) for severe/frequent headaches.
Relapse Prevention: Limit triptan, ergotamine-dihydroergotamine, or combination analgesic to \le\text{9} days/month; NSAIDs to \le\text{14} days/month.
Polymyalgia Rheumatica (PMR)
Overview: Inflammatory condition almost exclusively in people aged \ge\text{50} years. Peak incidence between ages \text{70} and \text{80} years.
Epidemiology: More common in females. Cause unknown.
Laboratory Findings: ESR mildly to severely elevated (\text{20\%} sedimentation rate \text{104 mm/hr}); CRP also elevated.
Association with GCA: High risk (\text{5\%}–\text{30\%}) of developing GCA. Educate patients on GCA symptoms.
Signs/Symptoms:
Bilateral joint stiffness and aching (\ge\text{30} minutes, commonly mornings) in posterior neck, shoulders, upper arms, and hips (pelvic girdle).
Pelvic girdle symptoms: groin pain, lateral hip pain radiating to posterior thigh.
Difficulty with activities like putting on clothes, hooking bra, getting out of bed/chair.
Severe morning stiffness ("gel phenomenon" – stiffness with inactivity) and pain lasting until afternoon if untreated.
Treatment Response: Symptoms usually respond quickly to oral steroids (e.g., prednisone daily).
Primary Headache: Cluster Headache (Detailed)
Overview: Idiopathic, severe, one-sided headache with recurrent episodes of severe, stabbing pain behind one eye, accompanied by autonomic symptoms.
Autonomic Symptoms (Ipsilateral): Lacrimation, nasal congestion, clear rhinitis, conjunctival injection (red eyes), ptosis (drooping eyelid), miosis (pupil constriction) – collectively can form Horner's syndrome.
Risk Factors: History of head trauma, tobacco use, familial history.
Onset: Abrupt onset; patient may be agitated during attack.
Pattern:
Episodic cluster bouts: Several times a day, recurring daily for weeks; alternating periods of attacks and remission.
Chronic cluster bouts: Continual attacks or brief remission (<3 months).
Rhythmicity: Relatively short-lived attacks (\text{15} minutes to 3 hours).
Resolution: Resolves spontaneously but may return.
Epidemiology: More common in adult males; typical onset between 20 and 40 years.
Severity: Can be debilitating; increased suicide risk due to severe pain intensity.
Classic Case: 35-year-old male with abrupt onset of recurrent brief, "ice-pick," severe, lacerating periorbital pain (above eye/brow or temporal area), accompanied by tearing and clear nasal discharge (rhinitis). May have ptosis. May pace the floor during acute attack.
Diagnosis: MRI scan recommended to exclude brain/pituitary abnormalities (e.g., aneurysms, AVM, pituitary macroadenoma, meningiomas).
Treatment Plan:
Acute Treatment:
High-Dose Oxygen: May relieve headache (\text{100\%} oxygen at \ge\text{12 L/min} by mask for \text{15} minutes). Avoid in severe COPD due to risk of hypercapnia/carbon dioxide narcosis.
Triptans: Sumatriptan (Imitrex) \text{6 mg} subcutaneous injection or intranasal. Intranasal zolmitriptan is another option.
Alternative Acute Therapies: Intranasal lidocaine, oral ergotamine, subcutaneous octreotide.
Prophylaxis:
Frequent Attacks: Verapamil (calcium channel blocker [CCB]) is drug of choice (\text{240 mg PO} daily initially). Avoid grapefruit juice. EKG monitoring if dose >\text{400 mg} due to risk of bradycardia, RBBB, complete heart block.
Infrequent Attacks: Preventive therapy with glucocorticoids alone.
Alternative Preventive Therapies: Galcanezumab, lithium, topiramate, greater occipital nerve blocks, pizotifen, valproate, capsaicin, triptans, ergotamine, melatonin, indomethacin.
Complications: Higher risk of suicide (in male patients).
Tips: Accompanied by eye redness and rhinorrhea; severe periorbital pain. Can occur several times a day. Spontaneously resolves. Common in middle-aged males. Treated with high-dose oxygen (caution in COPD).
Primary Headache: Migraine (Detailed)
Overview: Severe headache generally associated with nausea and/or light and sound sensitivity. Recurrent attacks often progress through four phases.
Phases:
Prodrome: Affective or vegetative symptoms \text{24-48} hours prior to headache onset (occurs in \text{77\%} of patients).
Aura: Focal neurologic symptoms (visual, sensory, language, motor disturbances) (occurs in \text{25\%} of patients).
Headache: Often unilateral with photophobia or phonophobia.
Postdrome: Symptoms of fatigue and exhaustion once headache resolves.
Epidemiology: More frequent in females (\text{17\%}) than males (\text{6\%}).
Most Common Type: Migraine without aura (\text{75\%}).
Children: Can present as abdominal pain.
Classic Case: Adult woman complains of gradual onset of throbbing headache behind one eye, gradually worsening over several hours. Reports sensitivity to bright light (photophobia) and noise (phonophobia). Frequently accompanied by nausea and/or vomiting (can be severe). Migraines last from \text{3} to \text{72} hours; many resolve during sleep.
Treatment Plan:
Nonpharmacologic Interventions:
Acupuncture.
Rest in a quiet, darkened room with an ice pack to forehead.
For nausea: ginger ale, cola, dry toast, saltine crackers.
Aerobic exercise.
Transcutaneous electrical nerve stimulation.
Avoid Precipitating Factors:
Nitrates/nitrites (hot dogs, luncheon meat, sausage).
Alcohol and caffeine.
Sleep changes, stress, barometric weather changes.
Odor triggers (tobacco smoke, perfumes, strong odors).
Visual triggers (strobe lights, sunlight, glares).
Emotional or physical stress.
Pharmacologic Options:
Mild-to-Moderate Attacks: Analgesics (acetaminophen or NSAIDs alone/combination) as first-line. If nausea/vomiting, prescribe antiemetic. Take pain medication ASAP.
Moderate-to-Severe Attacks: Oral triptans or combination sumatriptan–NSAID/naproxen (Treximet). If severe nausea/vomiting, non-oral agents (subcutaneous sumatriptan, nasal sumatriptan, zolmitriptan) with antiemetic.
Triptan Contraindications: Ischemic heart disease, Prinzmetal's angina, ischemic stroke, uncontrolled hypertension, hemiplegic/basilar migraine, pregnancy.
Triptan Side Effects: Flushing, tingling, chest/neck/sinus/jaw discomfort.
First Dose Precaution: Supervise first dose, especially if cardiovascular risk factors (diabetes, obesity, male >40 years, high lipids). Give first dose in office (theoretical MI risk). Consider EKG monitoring for high-risk heart disease patients.
Drug Interactions: Higher risk of serotonin syndrome if combined with SSRIs or SNRIs (duloxetine, venlafaxine). Do not combine or start within 2 weeks of MAOI use. Do not combine with ergots or within 24 hours of ergot use.
Calcitonin Gene-Related Peptide (CGRP) Antagonists: Rimegepant (Nurtec), ubrogepant (Ubrelvy). Do not mix with ketoconazole, itraconazole, clarithromycin. Do not mix with grapefruit juice or St. John’s wort. Many major drug interactions.
Serotonin 5-HT-1F Receptor Agonist: Lasmiditan (Reyvow). Can be used for patients with relative contraindication to triptans due to cardiovascular risk factors. Do not use within 8 hours of driving/heavy machinery (causes dizziness).
Ergots: Ergotamine preparations (alone or with caffeine/analgesics) for abortive treatment (e.g., dihydroergotamine [Migranal]).
Potent vasoconstrictors.
Do not mix with other vasoconstrictors (triptans, decongestants).
Common side effect: nausea.
Ergots and triptans should not be given within 14 days of an MAOI.
Antiemetics: Prochlorperazine (IM, IV, suppository, PO), trimethobenzamide (Tigan - IM, suppository, PO), ondansetron (Zofran - IM, IV, PO). Effective but not first-line.
Prophylactic Treatment: Indicated if headaches are frequent, long-lasting, or cause significant disability.
Beta-blockers: Propranolol (Inderal), metoprolol (Lopressor), nadolol (Corgard), atenolol (Tenormin).
CCBs: Verapamil (Verelan), flunarizine (Sibelium), nifedipine (e.g., Adalat) (efficacy overall weak).
ACE Inhibitors/ARBs: Lisinopril (Zestril), candesartan (Amias) (effective in smaller studies).
Tricyclic Antidepressants (TCAs): Amitriptyline (Elavil), nortriptyline (Pamelor).
SNRI: Venlafaxine (Effexor).
Anticonvulsants: Valproate (Depacon), topiramate (Topamax), gabapentin (Neurontin).
Tips: Migraines can last from \text{3} to \text{72} hours.
Primary Headache: Migraine with Brainstem Aura
Overview: Rare subset of migraine with aura, previously called basilar migraine.
Symptoms: Brainstem symptoms (dysarthria, vertigo, ataxia) without motor weakness. Resembles stroke but lacks hemiplegia. Focal neurologic findings (tinnitus, diplopia, bilateral visual symptoms, bilateral paresthesia) are part of the aura.
Headache: Followed by a throbbing occipital headache and nausea.
Consciousness: About \text{77\%} can have impairment in or loss of consciousness lasting \text{2} to \text{30} minutes.
Treatment: Similar to migraine headache with aura.
Tips: Distinguish abortive vs. prophylactic drugs. Answer options may list drug class.
Primary Headache: Tension-Type Headache (Detailed)
Overview: Bilateral, non-throbbing headache of mild to moderate intensity, typically without other features. Most prevalent headache.
Subtypes: Infrequent episodic (<1 day/month), frequent episodic (1 to 14 days/month), chronic (\ge\text{15} days/month).
Contributing Factors: Environment, genetic factors, heightened sensitivity of pain pathways in CNS (and likely PNS), muscular factors.
Classic Case: Adult patient complains of a headache that is "band-like," feels like "someone is squeezing my head." Pain is dull and constant, usually generalized, accompanied by tensing of neck muscles. Reports recent increased life stressors. Headache lasts several days.
Treatment Plan:
First-Line Analgesics: NSAIDs (naproxen sodium BID or ibuprofen QID) or aspirin every \text{4-6} hours. Acetaminophen if NSAID intolerance.
Alternative NSAID: Diclofenac TID if poor response to initial NSAIDs.
Pregnancy: Acetaminophen preferred.
Combination Drugs: Ibuprofen or aspirin with caffeine for inadequate relief from single agent.
Reevaluation: Reevaluate diagnosis if no response to initial treatment.
Avoid: Limit butalbital to \le\text{3} times/month. Opioids or butalbital not recommended as initial therapy. Muscle relaxants not recommended (lack of efficacy).
Stress Reduction: Yoga, tai chi, exercise, gradual caffeine reduction, regular eating/sleep schedule, counseling.
Tips: Most headaches (except tension) cause unilateral pain. Muscle tension causes vise-like or tight pain, may last for days.
Common Drugs: Headache Treatment
Acute Treatment (As Needed Only)
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs):
Naproxen sodium (Naprosyn, Aleve) BID or ibuprofen (Advil, Motrin) TID to QID.
Side effects: GI pain/bleeding/ulceration, renal damage, increased BP in hypertension.
Triptans:
Sumatriptan succinate (Imitrex) injection, inhalant, PO tablets, sublingual. Subcutaneous injection for acute pain (onset \text{10} minutes).
Side effects: Nausea, dizziness, vertigo, drowsiness; discomfort of throat, nose, tongue.
Contraindications: Cardiovascular comorbidities (vasoconstriction leading to coronary artery spasm, MI, transient myocardial ischemia), arrhythmias (atrial fibrillation, ventricular fibrillation, ventricular tachycardia).
Do not give within 24 hours of an ergot.
Do not give within 14 days of an MAOI.
Analgesics:
Acetaminophen (Tylenol) QID as needed.
Side effect: Hepatic damage.
Prophylaxis (Must be Taken Daily)
Tricyclic Antidepressants (TCAs):
Amitriptyline (Elavil), nortriptyline, doxepin, imipramine.
Side effects: Sedation, dry mouth, confusion in older adults.
Beta-Blockers:
Propranolol (Inderal LA) or atenolol (Tenormin) daily. Careful with older patients.
Contraindications: Second- or third-degree AV block, asthma, COPD, bradycardia.
Selective Norepinephrine and Serotonin Inhibitors (SNRIs):
Venlafaxine (Effexor) daily at bedtime. Consider if patient has migraine and depression, GAD, panic disorder, chronic anxiety.
Antiseizure Medications:
Topiramate (Topamax).
If discontinuing, withdraw gradually over a few weeks to minimize risk of seizures or withdrawal symptoms.
Treatment of Specific Headaches (Summary)
Migraines:
Acute: Ice pack, rest in quiet dark room, immediate analgesics, sumatriptan SC injection (or nasal spray for severe nausea), antiemetics (prochlorperazine).
Prophylaxis: Antihypertensives (beta-blockers, CCBs, ACEIs/ARBs), antidepressants (SNRI like venlafaxine, TCA like amitriptyline), anticonvulsants (topiramate, valproate, gabapentin).
Giant Cell Arteritis:
Acute: High-dose glucocorticoids.
Prophylaxis: Routine monitoring of disease activity and response.
Cluster:
Acute: Inhalation of \text{100\%} oxygen at \text{12 L/min} for \text{15} minutes, triptans (sumatriptan, zolmitriptan). Alternatives: intranasal lidocaine, oral ergotamine, IV dihydroergotamine.
Prophylaxis: Verapamil (for frequent attacks) or glucocorticoids (for less frequent attacks).
Trigeminal Neuralgia:
Acute/Initial: Carbamazepine (Tegretol) or oxcarbazepine.
Alternatives/Adjuncts: Gabapentin, lamotrigine, phenytoin, baclofen.
Prophylaxis: Continue medical therapy before gradual wean (goal: sustained pain-free interval of \ge\text{6-8} weeks). Watch for drug interactions.
Muscle Tension:
Acute: OTC analgesics (NSAIDs, acetaminophen), warm bath/shower, massage.
Prophylaxis: Stress reduction, yoga, relaxation, biofeedback.
Seizures
Prevalence: Affects \text{8\%} to \text{10\%} of the population. Intermittent, usually self-limiting.
Types:
Acute Symptomatic Seizure: Occurs during systemic insult or in close association with documented brain insult.
Unprovoked Seizures: Occur related to preexisting brain lesion or progressive nervous system disorder.
Categorization: Focal, generalized, or unknown (if onset missed/obscured).
Epilepsy: Characterized by recurrent, unprovoked seizures; can be focal or generalized.
Focal Seizures:
With Retained Awareness: Previously simple partial seizure; symptoms vary by cortical disruption.
With Impaired Awareness: Previously complex partial seizure; most common in adults with epilepsy. Patient appears awake but not in contact with environment.
Generalized Seizures:
Tonic-Clonic Seizure (Grand Mal): Most common generalized type. Abrupt loss of consciousness; extremities stiff (may appear cyanotic). Muscles jerk/twitch. Tongue may be bitten.
Absence Seizure (Petit Mal): Common in childhood; lasts \text{5-10} seconds; onset marked by behavioral arrest.
Atypical Absence Seizure: Longer, slower onset/offset; blank staring with impaired consciousness, change in muscle tone/movement, repetitive blinking.
Clonic Seizure: Rhythmic jerking muscle contractions (arms, neck, face).
Myoclonic Seizure: Sudden, brief muscle contractions (alone or in clusters); typically involves arms.
Tonic Seizure: Sudden muscle stiffening, often with impaired consciousness and falling.
Atonic Seizure (Drop Seizure): Sudden loss of muscle control, usually in legs, causing collapse.
Classic Case: Adult patient presents after abrupt onset of witnessed generalized tonic-clonic seizure. Experienced loss of consciousness, posture, muscle stiffness (arms, legs, chest, back), followed by brief, violent, generalized contractions with progressively longer muscle relaxation, foamy salivation, and tongue biting. Patient presents with confusion and suppressed alertness. Spouse describes due to patient's amnesia.
Treatment Plan:
Immediate Management: Airway assessment and stabilization of vital signs and airway.
History: Obtain detailed description of seizure and preceding events.
Lab Tests: CBC, serum electrolytes, blood glucose, calcium, magnesium, renal function, liver functions, UA, toxicology screen.
Diagnosis: Electroencephalogram (EEG) essential for epileptic seizure diagnosis.
LP: If concern for acute infectious process.
Imaging: MRI preferred over CT (superior sensitivity for causes of seizure/epilepsy).
Medication: Initiation of antiseizure medications (not always indicated after first unprovoked seizure).
Referral: To a neurologist.
Hospitalization Indications: First seizure with prolonged postictal state, incomplete recovery, serious seizure-related injury, status epilepticus, neurologic/systemic illness requiring attention.
Pharmacotherapy:
Antiseizure medication initiated in patients with \ge\text{2} unprovoked seizures.
Choice depends on patient-specific data, seizure type, other medications, comorbidities.
Over 25 approved medications: carbamazepine, clobazam, gabapentin, lamotrigine, levetiracetam, phenobarbital, phenytoin, topiramate, valproate.
Seizure Precautions:
Avoid common triggers: sleep deprivation, alcohol, infection, certain medications.
Avoid unsupervised dangerous activities: bathing, swimming alone, working at heights, operating heavy machinery.
Counsel patients on driving restrictions and specific limitations.
Transient Ischemic Attack (TIA)
Definition: Transient episode of neurologic dysfunction caused by focal ischemia (brain, spinal cord, or retinal) without acute infarction of the brain.
Evolving Definition: "Time-based" (resolution within \text{24} hours) replaced by "tissue-based" definition, recognizing permanent neurologic damage can occur with brief ischemia.
Urgency: Neurologic emergency and major warning sign. High risk for subsequent stroke; urgent evaluation and treatment needed.
Severity: Signs and symptoms vary from subtle to severe depending on intensity and duration. Longer TIA = higher risk of ischemic brain damage.
Typical TIA Symptoms: Transient, focal neurologic symptoms localized to a single vascular territory: transient monocular blindness, aphasia/dysarthria, hemianopia, hemiparesis, and/or hemisensory loss.
Atypical TIA Symptoms: Loss of some neurologic function.
ABCD2 Score: Clinical prediction tool to assess stroke risk after TIA within 7 days.
Factors and Points:
Age >\text{65} years: 1 point.
BP (first assessed after TIA): Systolic \ge\text{140} or Diastolic \ge\text{90}: 1 point.
Clinical Features (choose only 1):
Unilateral weakness with/without speech impairment: 2 points.
Speech impairment without unilateral weakness: 1 point.
Duration:
TIA duration >\text{60} minutes: 2 points.
TIA duration \text{10-59} minutes: 1 point.
Diabetes: 1 point.
Total ABCD2 Score Range: \text{0-7}.
Note: Predictive performance alone is not satisfactory; combine with other models, imaging, and etiology.
Classic Case: Older adult with acute onset of one-sided weakness (right arm/leg), dizziness, vertigo, poor balance. Speech is slurred (dysphasia). Right-sided facial weakness (lopsided smile). History of hypertension, atrial fibrillation, hyperlipidemia, type 2 diabetes. Symptoms eventually resolve, but patient remains at higher risk of future stroke.
Risk Factors for Recurrent Ischemic Stroke After TIA:
Age \ge\text{60} years.
History of TIA or ischemic stroke within 30 days of index event.
History of diabetes.
Systolic BP \ge\text{140 mmHg} OR diastolic BP \ge\text{90 mmHg}.
Unilateral weakness.
Isolated speech disturbance.
TIA duration >\text{10} minutes.
Presence of vascular pathologies (e.g., large artery atherosclerosis, small vessel disease).
Presence of acute infarction on MRI or acute/chronic ischemic lesions on CT.
"FAST" Mnemonic for Recognizing Stroke:
Face drooping: Instruct patient to smile. Is face lopsided?
Arm weakness: Instruct patient to raise both arms. Does one arm drift downward?
Speech difficulty: Instruct patient to say, "The sky is blue."
Time to call \text{911}: Even if symptoms go away, call \text{911}.
Hospitalization Criteria (First TIA within past 72 hours):
Known cardiac, arterial, or systemic etiology of brain ischemia amenable to treatment.
Acute infarction on MRI.
Concurrent serious acute medical issues.
Uncertainty of diagnostic workup completion within \text{24-48} hours in outpatient setting.
Treatment Plan:
Referral: To outpatient specialty TIA clinics or ED for evaluation to find cause (e.g., atrial fibrillation, carotid/vertebral atherosclerosis, hypercoagulable state, cocaine use, hypertension) and extent of brain damage.
Imaging: Schedule CT and/or MRI ASAP (within first \text{24} hours). MRI with diffusion-weighted imaging is superior, but non-contrast CT is standard for early acute stroke due to availability, speed, and ICH sensitivity.
Antiplatelet Therapy: Immediate initiation for TIA patients without known cardioembolic source. Exceptions: patients on oral anticoagulation or with new indication for anticoagulation.
Low-Risk TIA (ABCD2 score <\text{4}): Aspirin alone (\text{162} to \text{325 mg/day}).
High-Risk TIA (ABCD2 score \ge\text{4}): Dual antiplatelet therapy (DAPT) for first \text{21} days.
Aspirin (\text{160} to \text{325 mg} loading dose, then \text{50} to \text{100 mg} daily) PLUS clopidogrel (\text{300} to \text{600 mg} loading dose, then \text{75 mg} daily).
OR Aspirin (\text{300} to \text{325 mg} loading dose, then \text{75} to \text{100 mg} daily) PLUS ticagrelor (\text{180 mg} loading dose, then \text{90 mg} BID).
Cardiac Evaluation: EKG, continuous cardiac monitoring, echocardiography.
Lab Tests: CBC, coagulation panel, serum electrolytes and creatinine, fasting blood glucose, lipid panel, hemoglobin A1C, ESR, and CRP.
Intensive Risk Factor Management: Maintain BP <\text{140/90 mmHg}; LDL-C lowering with high-intensity statin; glucose control; physical activity; smoking cessation; weight reduction; adequate nutrition; alcohol reduction.
Trigeminal Neuralgia (Tic Douloureux) (Detailed)
Trigeminal Nerve (CN V) Divisions: Ophthalmic (V1), Maxillary (V2), Mandibular (V3).
Cause: Most cases caused by compression of the nerve root by an artery, vein, or tumor, leading to unilateral electric shock-like facial pain following one of the branches.
Pain Location: Usually near nasal border and cheeks, but can move.
Types: Classic, secondary (underlying disease), idiopathic.
Epidemiology: More common in women; most idiopathic/classic cases start after age \text{50}.
Classic Case: Older adult with sudden onset of severe, sharp, shooting pains on one side of the face or around the nose. Triggered by chewing, eating cold foods, cold air.
Severe lacerating (piercing knifelike) pain lasts a few seconds to 2 minutes.
Pain precipitated by stimulus on any area of the trigeminal nerve.
Patient may stop chewing/speaking momentarily.
Recurrent paroxysms of unilateral facial pain following CN V distribution.
Treatment Plan:
First-Line: Carbamazepine (Tegretol) or oxcarbazepine (Trileptal).
Alternatives/Adjuncts: Gabapentin (Neurontin), lamotrigine (Lamictal), or baclofen.
Rescue Therapy (while oral meds titrated): IV lidocaine, phenytoin, or fosphenytoin, or subcutaneous sumatriptan.
Imaging: Obtain MRI or CT scan to rule out tumor/artery pressing on nerve or MS.
Surgery: Indicated for medically refractory cases (e.g., microvascular decompression, rhizotomy, radiofrequency, nerve block).
Tip: Pain on one side of face/cheek, precipitated by talking, chewing, cold food, or cold air on affected area.