Exam 2
OBJECTIVES
Understand the etiology, incidence, and pathophysiology of commonly occurring acute neurological symptoms and disorders in adults.
Identify differential diagnosis of commonly occurring acute symptoms and disorders of the neurological system.
Know relevant subjective and objective data necessary to make an accurate diagnosis.
Identify appropriate diagnostic studies needed to establish an accurate diagnosis.
ACUTE NEUROLOGICAL DISORDERS
Headaches
Vertigo
Delirium
Seizures (Primary care management and workup)
Bell’s Palsy
DANGER SIGNALS
Acute bacterial Meningitis
Acute Stroke
Chronic Subdural Hematoma
Giant Cell Arteritis
Multiple Sclerosis
Subarachnoid Hemorrhage
MOST COMMON ACUTE NEUROLOGICAL PRESENTATION: HEADACHE
Goals of Evaluation of Headache
Identify and rule out life-threatening causes (secondary headache).
Example: sinus vs. meningitis - DANGER SIGNALS!
Correctly diagnose the etiology of the headache and identify any underlying disease or problem.
Provide symptom relief and help with prevention of future headaches.
TYPES OF HEADACHES
NON-EMERGENT
Migraine
Tension
Cluster
Mixed (combination headache)
Possible familial connections for migraine and hypertension.
EMERGENT - Red Flag HA
Giant Cell Arteritis
Subarachnoid Hemorrhage
Stroke
Infection
Primary and Secondary Headaches
Primary: migraine, tension, cluster.
Secondary: underlying pathology, “red flag” HA.
HEADACHE ASSESSMENT
Chronology: Most important history item.
Evaluate:
Location, duration, and quality of headache.
Associated activity: exertion, sleep, tension, relaxation.
Timing of menstrual cycle.
Presence of associated symptoms and triggers.
OFFICE VISIT ASSESSMENT - RED FLAGS IN PATIENT HISTORY
Sudden onset in seconds or minutes (thunderclap headache): SAH.
“First or worst” headache: hemorrhage or infection.
Focal neurological symptoms:
Focal = Movement changes: paralysis, weakness, loss of muscle control, increased or decreased muscle tone, involuntary movements (e.g., tremor).
Sensation changes: paresthesia or numbness.
Change in personality, mental status, or level of consciousness (non-focal).
TENSION HEADACHE
Most common type of headache (90% of all headaches).
Causes
Emotional/physical stress, mental tension.
Head and neck movements.
At-Risk Patients
Adults.
SIGNS/SYMPTOMS OF TENSION HEADACHE
Vise-like or tight quality.
Usually generalized.
May be most intense about the neck or back of the head.
No associated focal neurological symptoms.
Usually lasts for several hours.
Three Main Subtypes of Tension Headaches
Infrequent episodic: episodes last less than 1 day a month.
Frequent episodic: 1-14 days per month.
Chronic: 15 or more days per month.
Influencing Factors
Environmental and genetic factors.
Heightened sensitivity of pain pathways in the CNS (and likely PNS).
Muscular factors.
DIAGNOSTIC TESTING FOR TENSION HEADACHES
Mostly based on history, often supported by physical findings.
Clinical diagnosis, no specific labs required for tension headaches.
MANAGEMENT OF TENSION HEADACHES
Pharmacologic Options
OTC analgesics:
NSAIDs: Naproxen BID, ibuprofen QID, Aspirin Q4-6h.
Combination drugs (e.g., ibuprofen or aspirin with caffeine).
Example: Excedrin.
Limit use of Butalbital medications (Fioricet, Fiorinal) to no more than 3 times per month; current guidelines do not support these or opioids as first-line management.
Muscle relaxants not recommended due to lack of efficacy.
Non-Pharmacologic Management
Relaxation techniques: yoga, tai chi, exercise several times per week.
Gradually reduce caffeine.
Focus on sleep hygiene.
Counseling with a therapist.
MIGRAINE HEADACHES
EPIDEMIOLOGY
45% of headache visits are for migraine headaches.
Etiology
Primary neuronal dysfunction.
Significant racial differences in incidence; African Americans and non-white Hispanics are 2 times as likely as whites or Asians to be migraine sufferers.
Inverse relationship between migraine prevalence and age; highest between ages 20-40, lowest above 60.
Occurs in 4-5% of school-age children.
Migraines contribute to over 157 million workdays lost due to headache pain each year.
Often hereditary, particularly in women, and linked to hormonal shifts; genetic mutations associated with familial migraines in calcium-channel genes.
CAUSES/TRIGGERS OF MIGRAINES
Onset usually in adolescence or early adulthood.
Family history is common.
Females more affected than males.
Various Triggers Associated with Migraines
Emotional Factors: Stress (80%), hormones in women (65%), not eating (57%).
Physical Factors: Weather changes (53%), sleep disturbances (50%), alcohol (38%).
Environmental Factors: Odors (44%), neck pain (38%), lights (38%).
Food Triggers: Certain foods (27%), nitrates in cured foods.
PATHOPHYSIOLOGY OF MIGRAINES
Neuropeptide release.
Trigeminal nerve (CN V) activation leading to vasodilation, involving substances like VIP, substance P (Sub P), and calcitonin gene-related peptide (CGRP).
Plasma protein extravasation.
Activation of nociceptors.
TYPES OF MIGRAINES
Classic migraine: with aura.
Common migraine: without aura.
Characteristics
Historically attributed to dilation and excessive pulsation of branches of the external carotid artery.
Lasts between 2 to 72 hours, follows the trigeminal nerve pathway (CN V).
MIGRAINE SYMPTOMS
Unilateral, lateralized throbbing headache, episodic in nature.
Symptoms may include:
Focal neurological disturbances precede or accompany migraines (e.g., visual disturbances, aphasia).
Nausea and vomiting.
Photophobia and phonophobia.
4 PHASES OF A MIGRAINE
Prodrome: Affective or vegetative symptoms 24-48 hours prior to HA (77% of patients).
Aura: Focal neurological symptoms in 25% of patients occurring 5-60 min before HA.
Headache: Often unilateral, lasting 4-72 hours with associated photophobia.
Postdrome: Fatigue and exhaustion lasting 24-48 hrs post-headache.
DIAGNOSIS OF MIGRAINE
Diagnostic Criteria
Duration: HA lasts 4-72 hours.
Characteristics: 2 of the following:
Unilateral, pulsating quality.
Moderate to severe intensity.
Aggravated by routine activity.
N/V, photophobia, or phonophobia during the headache (at least 1).
Frequency: 5 or more attacks meeting these characteristics.
Migraine without aura: 2 attacks with aura symptoms.
Changes are fully reversible and develop over 5-60 minutes.
PATIENT ASSESSMENT FOR MIGRAINE
Often normal, but neurological deficits may be observed.
Careful neurological examination for focal deficits.
Requires thorough health history to rule out organic causes.
THOROUGH HX TO R/O EMERGENT HEADACHES
GCA - Giant Cell Arteritis
Consider in patients over 50, especially with new onset headache.
Symptoms include:
Severe headache (burning and throbbing).
Temporal or occipital pain.
Jaw claudication during chewing.
Possible visual loss or tenderness over affected artery.
Elevated ESR/CRP; temporal artery biopsy is gold standard for diagnosis.
DANGEROUS HEADACHES
Subdural hemorrhage, brain tumor, subarachnoid hemorrhage.
LABORATORY/DIAGNOSTICS
Testing Based on Hx and Presentation
Blood Chemistries, BMP, ESR (for GCA), CBC, CT scan of head (to rule out hemorrhage/hematoma).
VDRL, urinalysis, EEG not recommended as part of routine evaluation.
MANAGEMENT/TREATMENT FOR MIGRAINES
Non-Pharmacologic Treatment
Address known trigger factors (e.g., odors).
Relaxation/stress management techniques during acute attacks;
Rest in quiet, dark room with icepack.
Dietary adjustments (e.g., ginger ale for nausea).
Pharmacologic Management
Acute Migraine Management
Mild to Moderate Attacks: Simple analgesics (ASA, acetaminophen, ibuprofen) taken at onset may provide relief.
Persistent N/V: Anti-emetics should be administered.
Moderate to Severe Attacks: Utilize triptans, first line therapy.
Example: Imitrex (Sumatriptan) 6mg SQ at onset, can repeat in 1 hour.
Triptan Mechanism of Action
Acts as agonists at 5-HT receptors (1B and 1D).
Decreases neuropeptide release and causes vasoconstriction, thereby reducing pain or cutting off pain pathways.
ERGOTS FOR ACUTE MIGRAINE TREATMENT
Useful but should not be combined with triptans.
Example: Dihydroergotamine is more effective than ergotamine.
Contraindications for Ergots
Pregnancy, cardiovascular disease, hypertension, liver or kidney disease.
PROPHYLAXIS FOR MIGRAINES
For patients experiencing attacks 2-3 times a month.
Medications for Prophylaxis
Anticonvulsants:
Valproate, Topiramate (Topomax), Gabapentin.
Antidepressants:
TCAs: Amitriptyline (Elavil), Nortriptyline.
Beta Blockers:
Propranolol (Inderal), Metoprolol (Lopressor).
Botox: Onabotulinum for chronic migraine (31 injections every 12 weeks).
PATIENT EDUCATION FOR MIGRAINE MANAGEMENT
Prophylactic treatment for >2 attacks per month.
Encourage avoidance of triggers.
Importance of early treatment and diagnosis.
Caution with triptan overuse to prevent rebound headaches.
CLUSTER HEADACHES
EPIDEMIOLOGY AND CAUSES
Typically occur in middle-aged men with onset between ages 20 and 30.
Associated with seasonal clustering.
Most painful types of headaches within trigeminal cephalalgias, characterized by severe unilateral head pain and ipsilateral autonomic symptoms.
CLINICAL PRESENTATION
Characterized by stabbing pain behind one eye (termed “ice-pick” pain).
May follow alcohol ingestion and is characterized by severe unilateral periorbital pain.
Attacks usually occur at night, lasting under 2 hours with pain-free durations in between.
May include ipsilateral nasal congestion, rhinorrhea, and eye redness.
MANAGEMENT/TREATMENT OF CLUSTER HEADACHES
Individual attacks may require inhalation of 100% O2 for relief.
Triptans like Sumatriptan (Imitrex) at 6mg SQ may also be effective.
Prophylaxis can use Calcium Channel Blockers like Verapamil for chronic cluster headaches.
IMAGING WITH HEADACHES
When to Consider Imaging
“Red Flag” headaches.
Change in pattern, frequency, or severity of headache.
Worsening headaches despite therapy.
Unexplained neurological symptoms.
Onset of headache with exertion, cough, or during sexual activity.
New onset >50 years old.
Headaches associated with fever, stiff neck, cognitive changes, or personality changes.
VERTIGO
DIZZINESS AND VERTIGO: DIFFERENCES
Dizziness is a sensation of unsteadiness, faintness, light-headedness, and feeling of movement within the head.
Vertigo is a false sensation of rotation or movement (of the patient or surroundings) due to inner ear disease or vestibular disturbance.
Both conditions may be linked with nausea, vomiting, nystagmus, and unsteady gait.
CAUSES OF VERTIGO
PERIPHERAL VESTIBULAR - BPPV (Benign Paroxysmal Positional Vertigo)
Caused by dislodged calcium carbonate crystals in the inner ear, triggered by movement and lasting ~1 minute.
May reoccur over several weeks.
PERIPHERAL VESTIBULAR - MENIERE'S DISEASE
Caused by increased endolymph pressure; characterized by attacks lasting several hours, with hearing loss and tinnitus.
Not positional.
ACUTE VESTIBULAR NEURONITIS
Inflammation of the vestibular nerve usually following a viral infection, with acute onset lasting several weeks.
CENTRAL CAUSES OF VERTIGO
Non-positional causes (stroke, tumors, multiple sclerosis, vestibular migraine).
VERTIGO CATEGORIES AND DIFFERENTIAL DIAGNOSES
Acute, prolonged, severe, nonpositional (vestibular neuronitis, Meniere’s).
Recurrent spontaneous attacks (Meniere disease, vestibular migraine).
Chronic, persistent dizziness (stroke, tumor).
PHYSICAL EXAM/HISTORY AND PHYSICAL ASSESSMENT FOR VERTIGO
Patient may describe a sensation of room spinning; assessment may reveal nystagmus and associated symptoms like nausea and gait instability.
Maneuver: Dix-Hallpike test, the gold standard for BPPV.
TREATMENT/MANAGEMENT FOR VERTIGO
Medications for BPPV
Common Medications:
Meclizine (Antivert).
Dimenhydrinate (Dramamine).
Diphenhydramine (Benadryl).
Consultation/Referral
Generally necessary except for BPPV.
DELIRIUM
DELIRIUM VS DEMENTIA
Definitions
Delirium | Dementia |
|---|---|
Abrupt decline in cognitive function | Progressive cognitive decline over time |
Impaired attention and orientation | Generally preserved early in course |
Level of consciousness may vary | Usual state of functioning remains relatively stable |
Can be caused by medical conditions or drugs | Example: Alzheimer’s Disease |
DELIRIUM: DSM-5 DIAGNOSTIC CRITERIA
Criteria
A. Disturbance in attention and awareness; develops over a short period, usually hours to a few days.
B. Fluctuations in severity during the course of the day.
C. An additional disturbance in cognition (memory deficit, disorientation).
D. Evidence from history or exam showing that the disturbance is a direct physiological consequence of another medical condition or substance.
CHARACTERISTICS OF DELIRIUM
A reversible and temporary process, often with an abrupt onset.
Patients may exhibit excitability or irritability and have a short attention span or memory loss.
Typically secondary to medical conditions, drugs, or intoxications; requires prompt assessment and treatment.
RISK FACTORS FOR DELIRIUM
Common risk factors include:
Dementia and depression.
Elder abuse and falls.
History of delirium, malnutrition, and polypharmacy.
Sensory impairments and comorbidities (e.g., chronic pain, alcoholism, terminal illnesses).
CLINICAL ASSESSMENT FOR DELIRIUM
Comprehensive medication review.
Use of cognitive assessment tools (e.g., Mini-Cog, MOCA).
Monitor vital signs and perform cardiac assessments.
H&P Mnemonic for Assessment
Drugs: Review all medications for changes.
Electrolyte imbalances: check for dehydration or electrolyte disorders.
Lack of medication: withdrawal effects.
Intracranial problems: strokes, infections, hemorrhages.
Reduced sensory input: check for visual and auditory impairments.
Infection: most common infections in older adults.
Urinary: retention, incontinence, infections.
Myocardial issues: cardiac events may present as delirium.
LABS/IMAGING FOR DELIRIUM
Urinalysis and point-of-care testing; possible ordering of CBC, BMP, toxicology screens, and EKG.
Imaging should focus on emergent conditions over routine tests; CT/MRI may be done based on clinical presentation.
PREVENTION AND TREATMENT OF DELIRIUM
Focus on directed treatment aimed at the cause of delirium.
Implement strategies to mitigate risk: adequate orientation, cognitive stimulation, nutrition monitoring, mobilization, and reassessment of changes in the patient.
PHARMACOLOGY TREATMENT FOR DELIRIUM
Used as necessary after the primary etiology is identified and determined safe to address.
Medications: Haloperidol (Haldol) and Olanzapine (Zyprexa); monitoring is crucial due to potential side effects (e.g., extrapyramidal effects).
REFERRAL FOR DELIRIUM
Based on patient presentation, may require referral to specialists such as neurology or psychiatry for further evaluation.
SEIZURES
DEFINITIONS
Seizures consist of abnormal electrical activity, affecting 8-10% of the population; they are often intermittent and typically self-limiting.
Types:
Acute symptomatic: occurs at the time of systemic or documented brain insult.
Unprovoked: occurs without preceding brain insult.
Classification
Categorized as focal or generalized.
H&P AND PHYSICAL EXAM FOR SEIZURES
Initial patient assessment should include a thorough and detailed history of seizure episodes including:
Circumstances surrounding each seizure, precipitating factors, and patient risks.
Aura presence, prior CNS insults, and any positive family history.
LABORATORY/DIAGNOSTICS FOR SEIZURES
Important Tests
EEG: The most important test for classifying seizures.
CT/MRI: Needed for new onset seizures to rule out tumors.
Labs: CBC, electrolytes, glucose, and more as necessary.
TREATMENT/MANAGEMENT OF SEIZURES
Referral to a neurologist is essential.
Antiseizure medications may be indicated after two or more unprovoked seizures.
Common medications include:
Carbamazepine, Phenobarbital, Phenytoin, Valproic Acid.
FOLLOW-UP FOR SEIZURE PATIENTS
Risk for recurrence is greatest in the first two years.
Monitor lifestyle modifications regarding safety, restrictions (e.g., driving), and lifestyle changes to minimize recurrence.
BELL'S PALSY
RISK FACTORS
Diabetes, hypertension, toxins, infections (e.g., herpes simplex, shingles, Lyme Disease).
CLINICAL PRESENTATION OF BELL'S PALSY
Inability to close the eye resulting in irritation; asymmetrical facial muscle tone and smiles; sagging of the face.
Typically presents with weakness or complete paralysis on one side; sudden onset of symptoms within 1 week, with possible numbness but preserved sensation.
DIAGNOSIS AND TREATMENT
Diagnosis is idiopathic, often treated with corticosteroids over a 10-day course.
Acyclovir administration is suggested if herpetic etiology is suspected.
BELL'S PALSY - DIFFERENTIAL DIAGNOSIS
Consider choleastoma, salivary tumor, Guillain-Barre syndrome, Lyme disease, otitis media, Ramsay Hunt syndrome, sarcoidosis, and CNS lesions.
ACUTE BACTERIAL MENINGITIS
Symptoms
Acute onset of high fever, severe headache, stiff neck (nuchal rigidity), altered mental status, accompanied by petechial rash and vomiting.
ACUTE STROKE
Ischemic Stroke: Presents with one-sided paralysis, impaired speech, and facial weakness.
Hemorrhagic Stroke: Characterized by thunderclap headache, often linked with poorly controlled hypertension.
CHRONIC SUBDURAL HEMATOMA
Presentation
History of head trauma accompanied by headaches and gradual cognitive impairment (e.g., confusion, apathy, somnolence).
GIANT CELL ARTERITIS (GCA)
Warning Signs
New headaches or changes in pre-existing headache patterns in patients under 50, sudden visual disturbances, jaw claudication, and localized temporal artery tenderness or induration.
MULTIPLE SCLEROSIS
Symptoms
Episodic loss of vision, gait disturbances, diplopia, or sensory changes such as numbness/paraesthesia, urinary incontinence, and bowel incontinence.
SUBARACHNOID HEMORRHAGE
Key Indicators
Sudden rapid onset of a severe headache (“worst headache of my life”), possibly accompanied by nausea, vomiting, neck pain, photophobia, and changes in vision.
QUESTIONS AND TEST YOUR KNOWLEDGE
Example Questions
Which cardiac drug is used for prophylactic migraine management?
Options: Beta blockers, Nitrates, ACE inhibitors, Alpha-adrenergic blockers.
A patient with chronic headaches is assessed; the likely diagnosis?
Options: Tension headache, Migraine headache, Cluster headache, Potential brain tumor.
Risk factor for recurrent ischemic stroke after TIA?
Options: Age 50, Hyperlipidemia history, BP after TIA, Duration of TIA symptoms.
A patient experiences throbbing headache with visual disturbances related to external factors?
Options: Alcohol, Overeating, MSG, Chewing.
Other Example Questions
Contraindications for prescribing triptans include?
Which diagnostic procedures are appropriate for patients with presentations of delirium?