CLINICAL CARE OF THE NERVOUS SYSTEM Flashcards

Question

``` DETERMINE THE MANAGEMENT OF A PATIENT WITH CLOSED HEAD INJURY TO INCLUDE ANEURYSM Intracranial Hemorrhage (ICH) 1. Type depend on where bleeding occurs 2. Epidermal Hemorrhage 3. Epidermal Hemorrhage 4. Epidural Hemorrhage Presentation 5. Epidural Hematoma Acute Management 6. Complications of Epidural Hematoma 7. Epidural Hematoma Disposition 8. Subdural Hemorrhage 9. Subdural Hematoma Pathophysiology 10. Subdural Hematoma Clinical Manifestations 11. Subdural Hematoma Acute Management 12. Subarachnoid Hemorrhage Epidemiology 13. SAH Clinical Presentation 14. SAH Treatment 15. Complications of SAH ```

Answer 1

(1) Type depend on where bleeding occurs (a) Epidural hematoma - between dura mater and skull (b) Subdural hematoma – between dura mater and arachnoid mater (c) Subarachnoid hematoma – between arachnoid mater and pia meter 1) High association with aneurysms or AV malformations (d) Intracerebral bleed (2) Epidermal Hemorrhage- Epidemiology (a) 1-4% of head trauma cases (b) Uncommon, but serious complication (c) Highest among adolescents (d) Rare in patients >50 years (e) Usually caused by traffic accidents, falls, and assaults (f) 75-95% have associated skull fracture (3) Epidural Hemorrhage - Pathophysiology (a) 85% of the time, skull fracture leads to arterial injury (b) Middle meningeal artery commonly affected (c) Normally the epidural space is a potential space, with the dura tightly attached to the skull (d) Under arterial pressure, the dura slowly peels away and a blood pocket forms (4) Epidural hemorrhage presentation (a) Classic picture involves: 1) Immediate loss of conciousness after significant head trauma 2) “Lucid interval” with recovery of consciousness (b) After a period of hours, increasing headache with deteriorating neurologic function (c) May also see seizure, coma, anisocoria, respiratory collapse (d) Evaluation incudes H&P, complete and serial neuro exams, and examination of eyes for papilledema (5) Epidural hematoma acute management (a) Oxygenation, prepare/initiate intubation if GCS < 8 (b) Immediate neurosurgical consultation (operation likely required- trephination, burr hole) (c) Closely monitor neurologic signs for increased ICP/herniation (6) Complications of epidural hematoma (a) Coma (b) Respiratory depression (c) Death unless treated by surgical evacuation (7) Epidural hematoma disposition (a) MEDEVAC for immediate neurosurgical consultation and Head CT. (8) Subdural Hemorrhage (a) More common than epidural, 20% of severe head injuries (b) Elderly, EtOH abusers, anticoagulated at risk (c) Underlying brain injury is often severe (d) May occur without impact (e) Dismal prognosis - 60% mortality (9) Subdural hematoma pathophysiology (a) Acceleration in the lateral direction tears briding veins draining the brain to the dural sinuses (b) Lower pressure blood, but actual rather than potential space (c) May tamponade resulting in gradual progression (d) May be chronic (10) Subdural hematoma clinical manifestations (a) May or may not have history of head trauma (b) Acute subdural hematoma presents 1-2 days after onset 1) May have lucid interval after injury (c) Chronic subdural hematoma presents 15 days or more after onset (d) Insidious onset of headaches, light headedness, cognitive impairment, apathy, somnolence are typical symptoms (11) Subdural hematoma acute management (a) Same as epidural hematoma (b) Non-contrast CT can help make differentiation between epidural and subdural hematoma (12) Subarachnoid Hemorrhage (SAH) epidemiology (a) Usually rupture of blood vessel aneurysm (~80%) (b) Sometimes trauma or congenital anomaly (c) Bleeding is high pressure and into subarachnoid space which normally carries CSF (13) SAH clinical presentation (a) Hallmark “Thunder clap headache” or “worse headache of my life” (b) Headache onset is sudden and may have meningeal irritation 1) Blood from cerebral blood vessels irritates the brain and meninges (c) Prior to onset patient may have been doing activity that increased intrathoracic pressure (d) Activities that increase risk of SAH 1) Drug use (cocaine, amphetamines), smoking, hypertension, alcohol use (14) SAH treatment (a) Bedrest (b) Analgesia with Tylenol (c) Avoid drugs that can lead to anticoagulation (d) MEDEVAC (15) Complications of SAH (a) Very high mortality rate (51%) (b) Rebleeding (7%) only eliminated by treating underlying cause (c) Cerebral ischemia (30-40%) either by loss of blood flow or vasospasm (d) Increase ICP (54%) includes due to increase blood volume and swelling from inflammation (e) Seizures (7%), Hyponatremia, Cardiac arrhythmias

Answer 2

(1) Injury: Physical Damage to the body or body part of the Service member? (Yes/No) (2) Evaluation: (a) H - Headaches and/or vomiting? (Yes/No) (b) E - Ear ringing? (Yes/No) (c) A - Amnesia, altered consciousness, and/or loss of consciousness? (Yes/No) (d) D - Double vision and/or dizziness? (Yes/No) (e) S - Something feels wrong or is not right? (Yes/No) (3) Distance: Was the Service member within 50 meters of the blast? (Yes/No) (a) Record the distance from the blast. (b) Service members will be referred for a medical evaluation if involved in a potentially concussive event as defined in section 1 of this enclosure, if there is a "Yes" response on the I.E.D. Checklist, or if they demonstrate any of the symptoms listed at any point after an injury event.

Answer 3

(1) Potentially Concussive Event. (a) Potentially Concussive Event. (b) Service members involved in a potentially concussive event as described in section 1 of this enclosure are required to rest for 24 hours, beginning at the time of the event. (2) First Diagnosed Concussion (a) All Service members diagnosed with a mTBI/concussion must have, at a minimum, 24 hours' recovery unless the results of subsequent clinical evaluation indicate a longer period is needed. (3) Second Diagnosed Concussion (Within a 12- month Period). (a) If two diagnosed mTBI/concussions have occurred within the past 12 months, return to duty is delayed for an additional 7 days following symptom resolution. (4) Recurrent Concussion (Within a 12-month Period) (a) If three diagnosed mTBI/concussions have occurred within the past 12 months, return to duty is delayed until a recurrent concussion evaluation has been completed. (5) MTBI/Concussion Screening and Initial Evaluation. (a) Use section one of the Military Acute Concussion Evaluation (MACE) to complete the initial screening of Service members involved in a potentially concussive event. (6) Refer to and direct trainee to refer to Military Acute Concussion Evaluation (MACE), Current edition, via eCampus or via handout.

Answer 4

(1) Comprehensive Neurological Evaluation (2) Neuroimaging (3) Neuropsychological Assessment: (a) Domains that can be affected by concussion and should be evaluated: 1) Attention 2) Memory 3) Processing speed 4) Executive functioning (4) Functional Assessment (5) Duty Status Determination

Answer 5

a. Presentation (1) Injury to the spinal cord results in characteristic neurologic symptoms. (2) Related to the pattern of tracts that are present in spinal cord anatomy. b. Epidemiology (1) 40 million persons per year affected (2) MVA (47%), Falls (23%), Violence (14%), Sports (9%) (3) Largely affects young male c. Pathophysiology of spinal cord injury (1) Most traumatic spinal cord injuries occur with injury to vertebral column which leads to mechanical compression of the spinal cord (2) Mechanical compression can lead to ischemia and inflammation d. Presentation of spinal cord injury (1) Depends on spinal cord level affected (2) Immediately after injury there may be complete physiologic loss of all spinal cord function below level of injury (a) Flaccid paralysis (b) Anesthesia (c) Absent bowel or bladder control (d) Loss of reflex activity (3) Physiologic loss can be transient and there may be recovery (4) Delayed symptom onset can occur due to spinal cord swelling e. Treatment and management of spinal cord injury (1) Should always focus on ABCs first (2) Take care to immobilize the C-spine with cervical collar ASAP (3) Patient with high cervical injury may have poor respiratory function and may require intubation if necessary (4) Maintain oxygenation and blood pressure (5) Insert a Foley catheter if bladder paralysis is suspected (6) Sedate patient if necessary (7) Steroid use is controversial, consult with Medical Officer prior to administration. Theoretically decreases swelling and inflammation after cord injury. (a) Methylprednisolone (Solumedrol) 125mg IM/IV q 4-6 hours prn 1) MOA: Anti-inflammatory; inhibits multiple inflammatory cytokines 2) Adverse Reactions: Adrenal insufficiency, steroid psychosis, infection, increased blood sugars, arrhythmias, HTN, GI bleeding, GERD 3) Contraindications: Hypersensitivity to milk protein, severe infection, hypertensive urgency/emergency (8) MEDEVAC ASAP! (a) C-spine CT and Neurosurgical Consultation (9) NEXUS Criteria for C-Spine XR (a) If any of these present, then C-spine x-ray should be done: 1) N: Focal Neurological deficit 2) S: Midline Spinal tenderness 3) A: Altered mental status 4) I: Intoxicated 5) D: Distracting injuries

Answer 6

(1) Radiculopathy overview (a) Lumbar disk herniation is usually due to bending or heavy loading (e.g., lifting) with the back in flexion, causing herniation or extrusion of disk contents (nucleus pulposus) into the spinal cord area. (b) However, there may not be an inciting incident. (c) Disk herniations often occur from degenerative disk disease (desiccation of the annulus fibrosis) in patients between 30 and 50 years old. (d) The L5-S1 disk is affected in 90% of cases. (e) Compression of neural structures, such as the sciatic nerve, causes radicular pain. (f) Severe compression of the spinal cord can cause the cauda equina syndrome, a surgical emergency. (2) Radiculopathy clinical presentation (a) Pain with back flexion or prolonged sitting (b) Radicular pain into the leg due to compression of neural structures (c) Lower extremity numbness and weakness (d) Discogenic pain typically is localized in the low back at the level of the affected disk and is worse with activity. (e) Sciatica” causes electric shock- like pain radiating down the posterior aspect of the leg often to below the knee. (f) A significant disk herniation can cause numbness and weakness, including weakness with plantar flexion of the foot (L5/S1) or dorsiflexion of the toes (L4/L5). (g) The cauda equina syndrome should be ruled out if the patient complains of perianal numbness or bowel or bladder incontinence. (pts with a traumatic injury or radicular pain) (h) Clinical presentation depends on level of herniation 1) L1- pain, paresthesia and sensory loss in the inguinal region 2) L2, L3, L4 – acute back pain that radiates around anterior aspect of thigh to knee and may have weakness of hip flexion, knee extension and hip adduction 3) L5 – most common radiculopathy; back pain radiating down lateral aspect of the leg into the foot and decreased strength in foot dorsiflexion, toe extension, foot inversion, foot eversion 4) S1 – pain radiating down posterior aspect of leg into the foot. Weakness in plantar flexion due to gastrocnemius. (3) Physical examination (a) Straight leg testing (89% of people with positive findings have herniated discs [not on TG]) 1) Lay patient supine and raise patients extended leg on the symptomatic side with foot dorsiflexed 2) Lasegue’s sign – presence or worsening of radicular pain with straight leg maneuver (4) Imaging (a) Plain radiographs are helpful to assess spinal alignment (scoliosis, lordosis), disk space narrowing, and OA changes. (b) MRI is the best method to assess the level and morphology of the herniation and is recommended if surgery is planned. (5) Treatment (a) First-line treatments include modified activities; NSAIDs and other analgesics (b) Muscle relaxants can help with acute symptomatic relief 1) Cyclobenzaprine (Flexeril) 5mg PO Q8Hr and can increase dose to 7.5 – 10mg (c) Reevaluation of the patient 4-6 weeks should occur (d) If pain is persistent at reevaluation then further adjunctive treatments should be considered (physical therapy) (e) If physical therapy is unsuccessful then consult to pain management or surgery should be considered depending on severity of symptoms (f) Following nonsurgical treatment for a lumbar disk for over 1 year, the incidence of low back pain recurrence is at least 40% and is predicted by longer time to initial resolution of pain.

Answer 7

a. Overview of Cauda Equina Syndrome (1) The cauda equina is a bundle of nerves that spread out from the bottom of the spinal cord (2) Cauda equina syndrome is the medical term for a group of symptoms that happen when some of the nerves in the cauda equina get squeezed or damaged. b. Pathophysiology (1) A herniated disc - The material from a ruptured disc can press on or irritate the nerves in the cauda equina (2) Infection or inflammation - Different types of infection or inflammation can damage or irritate nerves in the cauda equina. (3) Cancer - In people with cancer, tumors can form within the spine and press on the nerves in the cauda equina. (4) Spinal stenosis - Spinal stenosis is a condition in which the vertebrae form bumps called bone spurs. These bumps can squeeze or press on the nerves in the cauda equina. In people with spinal stenosis, the discs between the vertebrae also tend to dry up and shrink. That causes the space between the vertebrae to get smaller, sometimes pinching nerves. c. Clinical presentation (1) Pain, numbness, or tingling in the lower back and spreading down 1 or both legs (2) Leg weakness or a problem called "foot drop," which is when you cannot seem to hold your foot up (for example, while walking) (3) Problems with bowel or bladder control (4) Problems with sex d. Treatment (1) Cauda equina syndrome is a medical emergency. (2) Likely needs MRI for assessment (3) Treatment for cauda equina syndrome involves treating whatever is affecting the nerves and causing the symptoms. (4) Often, that means having surgery to remove bits of bone or discs, or tumors. (5) If the cause is an infection or inflammation, medications to treat those problems might be needed.

Answer 8

a. Essentials of the Diagnosis of Mononeuropathies (1) Focal motor or sensory deficit. (2) Deficit is in territory of an individual peripheral nerve. (3) An individual nerve may be injured along its course or may be compressed, angulated, or stretched by neighboring anatomic structures, especially at a point where it passes through a narrow space (entrapment neuropathy). (4) Pain is commonly felt distal to the lesion. (5) The precise neurologic deficit depends on the nerve involved. (6) Percussion of the nerve at the site of the lesion may lead to paresthesia in its distal distribution. (7) In chronic compressive or entrapment neuropathies, avoidance of aggravating factors and correction of any underlying systemic conditions are important. b. Carpal Tunnel Syndrome overview (1) An entrapment neuropathy caused by compression of the median nerve between the carpal ligament and other structures within the carpal tunnel. (2) Can be caused by repetitive wrist activities. (3) Commonly seen during pregnancy and in patients with diabetes mellitus or rheumatoid arthritis. c. Carpal tunnel syndrome presentation (1) Pain, burning, and tingling in the distribution of the median nerve. (a) Median nerve innervates thumb, pointer, middle and half of the ring finger (2) Initially, most bothersome during sleep. (3) Late in the syndrome weakness or atrophy of the thenar eminence may occur d. Carpal tunnel syndrome diagnosis (1) Tinel or phalen’s sign exacerbates neuropathic symptoms (2) Diagnosed with ultrasound and nerve conduction studies. e. Carpal tunnel syndrome treatment (1) Patient should modify their hand activities and the affected wrist should be splinted in neutral position for up to 3 months. (2) Oral or injected steroids or NSAIDS can help decrease inflammation and lesson pain. (3) Refer if symptoms persist more than 3 months despite conservative treatment, including the use of a wrist splint OR if thenar muscle (e.g., abductor pollicis brevis) weakness or atrophy develops. (4) Treatment is directed toward relief of pressure on the median nerve.

Answer 9

a. Overview of Bell’s Palsy (1) Acute facial palsy (paralysis) of a specific pattern (2) Lower motor neuron disease affecting CN VII (3) Rare (34/100,000 people) and slightly more common in pregnancy, otherwise no predisposing factors. (4) Idiopathic paresis of lower motor neuron type (5) Associated with Herpse Simplex Virus, Lyme disease, HIV and sometimes idiopathic b. Clinical presentation (1) Abrupt onset of unilateral facial paralysis (2) Pain about the ear precedes or accompanies the weakness in many cases but usually lasts only for a few days. (3) Face feels stiff and pulled on one side (4) May be ipsilateral restriction of eye closure and difficulty with eating and fine facial movements. (5) May have changes in taste (6) Tearing (68%) or dryness of the eye (16%) and less frequent blinking on the affected side (7) Bell's phenomenon (upward rolling of the eye on attempted lid closure) c. Diagnosis of Bell’s Palsy (1) Clinical diagnosis d. Seizure vs. stroke (1) In a stroke, there is NO paralysis of the forehead (2) Intact forehead muscle tone suggests STROKE not BELL’s Palsy (3) Look for other abnormalities or neurological deficits e. Treatment of Bell’s Palsy (1) Evaluate eye closure (a) If there is inadequate closure eye protective measures should be implemented (2) Can shorten duration of symptoms with oral steroids (3) Prednisone is used for mild to moderate Bell’s Palsy (a) Dose: 60mg PO daily x7 days, then 5 day taper, best to start within 5 days of symptoms (b) MOA: Inhibits multiple inflammatory cytokines, inhibits both COX1 and COX2 enzymes (c) Adverse Reactions: Adrenal insufficiency if taken longer than 7 days in a row, Cushing syndrome with long term use, HTN, GI bleeding, emotional lability (d) Contraindications: Systemic fungal infection, TB infection, HTN uncontrolled, CHF, uncontrolled DM (4) Antiviral medication is added to steroid treatment regimen for severe Bell’s palsy (a) Valacyclovir 1000mg 3 times daily for 7 days f. Differential Diagnosis (1) Herpes zoster (2) Otitis Media (3) Lyme disease (4) Guillain-Barre syndrome g. Prognosis (1) 60% of all cases recover completely without treatment (2) 10% of all patients remain disfigured h. Complications: (1) Long term or permanent disfigurement and problems with CN VII (2) Corneal ulceration (use artificial tears, lubricating ointment, and possible eye shield) i. Disposition: (1) Immediate referral/MEDEVAC, if eye complications or suspicious of alternative diagnosis (i.e. CVA) (2) Referral to neurology/MEDADVICE if mild paresis and no other symptoms to suggest alternative diagnosis (3) While onboard follow symptoms and extent of paralysis

Answer 10

a. Overview of Meningitis (1) Definition of Meningitis: Inflammation of the coverings of the brain(meninges) (2) Meninges consist of the dura mater, arachnoid mater, pia mater (3) Unlike the brain the meninges have nociceptors (4) May be viral or bacterial, spirochete or fungal etiology (5) One of the 10 most common infectious causes of death (6) Fatality rate 25% with 28% of survivors having permanent neurologic morbidity b. Common bacterial etiologies (1) Streptococcus pneumonia (2) Neisseria meningitides (3) Listeria monocytogenes c. Common viral etiologies (1) Enterovirus (2) Herpes simplex virus (a) Between 13-36% of patients presenting with primary genital herpes may have findings consistent with meningeal involvement. 1) Headache, photophobia, meningismus (3) West Nile Virus d. Signs and symptoms of meningitis (1) Classic triad of acute bacterial meningitis (a) Fever (b) Nuchal rigidity (c) Change in mental status (2) Nuchal rigidity due to meningeal irritation (3) Other symptoms (a) Headache (b) Photophobia (c) Rash (associated with Neisseria meninitidis) (4) Meningitis vs encephalitis (a) Important distinguishing feature is degree of brain function disturbance (b) In meningitis cerebral function usually remains normal (c) Encephalitis brain function is more abnormal leading to altered mental status, motor and sensory deficits, altered behavior, speech or movement disorders, speech changes e. Diagnosis of meningitis (1) Test meningeal irritation (a) Brudzinski sign – spontaneous flexion of hips during passive flexion of the neck (b) Kernig sign – inability or reluctance to allow full extension of knee when hip is flexed at 90 degrees (2) Lab testing (a) Lumbar puncture to evaluate CSF (b) LP should be delayed if there are signs of increased intracranial pressure 1) Papilledema 2) Focal neurological deficit 3) Abnormal level of consciousness (c) Initiation of treatment should not be delayed if there is high clinical suspicion of meningitis. f. Acute Management and treatment (1) Medical emergency with close to 100% fatality rate if left untreated (2) Need antibiotics that can cross blood-brain barrier (3) Empiric treatment covers most common bacterial etiologies and focuses on decreasing acute inflammation. (a) Ceftriaxone (rocephin) 1) Dose: 2g IV Q12Hr 2) MOA: Bactericidal; inhibits cell wall mucopeptide synthesis 3) If patient has a penicillin allergy consult the MO prior to administration due to cephalosporin and penicillin cross reactivity. (b) Vancomycin (not in AMAL) (c) Dexamethasone 1) Dose: 0.15mg/kg IV Q6Hr 2) Decreases acute inflammation in CNS 3) Studies demonstrate that there are less neurological long term complications (d) If aseptic meningitis due to HSV is suspected (eg, concomitant genital lesions), empiric therapy with acyclovir IV is recommended (e) Prophylaxis 1) Exposed crew – Ciprofloxacin (Cipro) - is a Fluoroquinolone antibiotic a) Dose: 500 mg PO x1 b) MOA: Bactericidal; inhibits DNA gyrase and topoisomerase IV c) Adverse Reactions: Photosensitivity, serum sickness, seizures, tendon rupture, nephrotoxicity d) Contraindications: QT prolongation, G6PD deficiency, tendon disorder, renal impairment, hepatic impairment, seizures 2) Mask patient and medical personnel in close proximity 3) Ensure vaccinations are current a) Meningiococcal, S. penumoniae, and H. influenza vaccinations

Answer 11

a. Overview (1) Chronic pain can be classified into 3 categories (a) Nociceptive pain 1) Pain caused by a stimuli that threaten or result in bodily tissue damage (b) Neuropathic pain 1) Pain resulting from maladaptive response to damage or pathology of the somatosensory nervous system 2) Can occur in absence of active stimuli or as an exaggerated response to minor or moderate stimuli (c) Centralized pain 1) Reduced ability of the CNS to diminish responses to peripheral stimuli (2) Common complaints are low back pain, joint pain, severe headache, neck pain, facial pain (3) Chronic pain affects all aspects of life from family life to employment b. What is pain? (1) Unpleasant sensory and emotional experience associated with actual or potential tissue damage (2) Pain is experienced in developmental, social and emotional context therefore evaluation of patients with chronic pain requires a search for a biomedical cause, psychologic and social evaluation and assessment of physical function and sleep (3) Chronic pain is defined as an acutely painful condition that persists beyond the usually expected 6-12 week time course for healing c. Neuropathic pain vs nociceptive pain (1) Nociceptive pain is characterized by what we traditionally recognize as a pain that is caused by a noxious stimuli (2) Neuropathic pain is most commonly described as tingling, pins and needles, burning, shooting electric like shocks d. Patient evaluation (1) Thorough evaluation includes: (a) Past medical and surgical hx (b) Review of systems (c) Social and family hx (d) Psychiatric hx (e) Pain assessment: Hx of pain, location, characteristics, severity and impact of daily life e. Imaging (1) Imaging may be useful when pain is in a specific site of bone or joint f. Management and treatment of chronic pain (1) Initial management is with non-pharmacologic therapies (a) Home exercise programs (b) Physical therapy (2) Psychological approaches especially for patients with mood, sleep, quality of life or interpersonal relationship issues (a) Cognitive behavioral therapy (CBT) (b) Mindfulness therapy (3) Other treatment (a) Acupuncture (b) Spinal manipulation with osteopathic manipulation therapy or chiropractic care (c) Transcutaneous nerve stimulation (TENS) (4) Medications (a) Medications that inhibit pain transmission 1) Tylenol 2) NSAID 3) Capsaicin (b) Medications that inhibit descending pain modulation 1) Gabapentin 2) Tricyclic antidepressants 3) SNRIs (5) Important to set patient expectations (a) Patients should be educated on realistic expectations for response (b) Chronic pain Is rarely fully eliminated but often can be reduced 1) On average there is a 30% reduction in pain which can help to improve quality of life and function (c) Important to give reassurance and have proper follow up with this patient population

Answer 12

a. Overview (1) Sleep consists of two distinct states as shown by electroencephalographic studies: (a) NREM – quiet sleep 1) Stage 1: Beginning of sleep cycle; light stage that is the transition between wakefulness and sleep 2) Stage 2: Become less aware of surroundings; breathing and heart rate becomes more regular; people spend ~50% in this stage 3) Stage 3: Deepest sleep stage; muscles relax and people are less responsive to noise and activity; delta wave sleep (b) REM – Dreams occur in this stage and brain is more active; eyes move rapidly; “paradoxical sleep” (2) Sleep is a cyclic phenomenon, with four or five REM periods during the night accounting for about one-fourth of the total night's sleep (1.5-2 hours). (3) The first REM period occurs about 80-120 minutes after onset of sleep and lasts about 10 minutes. (4) Later REM periods are longer (15-40 minutes) and occur mostly in the last several hours of sleep. Most stage 4 (deepest) sleep occurs in the first several hours. (5) Variations in sleep patterns may be due to circumstances ("jet lag") or to idiosyncratic patterns ("night owls") in persons who perhaps because of different "biologic rhythms" habitually go to bed late and sleep late in the morning. (6) Creativity and rapidity of response to unfamiliar situations are impaired by loss of sleep. b. Insomnia clinical features (1) Difficulty initiating or maintaining sleep (a) Common complaints of poor sleep quality or insufficient quantity due to difficulty initiating sleep or maintaining sleep (2) Risk factors that can lead to sleep issues (a) Alcohol abuse – alcohol decreases REM sleep (b) Stimulant abuse – preworkout or caffeine (c) Tobacco abuse (d) Psychiatric comorbidities (3) Compromised daytime function (a) Fatigue or malaise (b) Poor attention of concentration (c) Mood disturbance (d) Daytime somnolence (e) Reduced motivation of energy (4) Frequently coexists with medical, psychiatric, sleep, neurological disorders c. Diagnosis of insomnia (1) Chronic diagnosis established by history and patient report (2) Sleep history for 1 week (a) Detailed description of sleep problems 1) Number of awakening and durations of awakening 2) Sleep time and duration 3) Symptoms of disturbed sleep like daytime somnolence or fatigue (3) Diagnostic criteria (a) Requires that the 4 following criteria are met 1) Difficulty initiating sleep, maintaining sleep or waking up too early 2) Sleep difficulties occur despite adequate opportunity for sleep 3) Patient has daytime impairment that is attributable to sleep difficulty 4) Sleep difficulty is not better explained by another sleep disorder or substance abuse d. Differential diagnosis (1) Restless legs syndrome (2) Sleep apnea (3) Depression e. Treatment (1) Shot term insomnia (less than once month in duration) (a) Usually occurs from psychologic or physiologic stress (b) Educate and reassurance may be all that is needed (c) Educate on sleep hygiene 1) Consistent bedtime and wake time 2) Attempt to sleep should only occur if patient is sleepy 3) Avoid napping and dozing during the day 4) Avoid “clock watching” 5) Avoid electronics before bedtime 6) Avoid stimulants, tobacco, alcohol right before bed (2) Chronic insomnia (a) Psychological sleep referral for cognitive behavior therapy (3) Medication (a) Medications should not be the sole treatment of insomnia (b) Benzodiazepines have been the most widely prescribed true sedative hypnotics, being safer than barbiturates though they are best for short term use. (c) Melatonin 1) Dose: 3-5mg PO qHS 2) Side effects: Vivid dreams and nightmares, daytime somnolence, GI irritability (d) Trazodone 1) Dose: 50mg PO qHS 2) MOA: Inhibits reuptake of serotonin, causes adrenoreceptor subsensitivity, acts as a 5HT2a receptor antagonist and induces significant changes in 5-HT presynaptic receptor adrenoreceptors; significantly blocks histamine (H1) and alpha1- adrenergic receptors. 3) Side effects: Blurred vision, syncope, edema, weight loss (e) Vistaril 1) Dose: 25-50mg PO qHS 2) MOA: Competes with histamine for the 5HT2 and dopaminergic receptors in the hippocampus (f) Diphenhydramine 1) Dose: 25-50mg PO qHS f. Prognosis (1) Depends on the underlying cause of insomnia as well as the prevention of secondary complications such as substance misuse in the context of self-medication.

Answer 13

a. Overview of vertigo (1) Either a sensation of motion when there is no motion or an exaggerated sense of motion in response to movement. (2) Must differentiate peripheral from central etiologies of vestibular dysfunction. (a) Peripheral: Onset is sudden; often associated with tinnitus and hearing loss; horizontal nystagmus may be present. 1) Etiologies: a) BPPV b) Herpes zoster c) Otitis media d) Aminoglycoside toxicity (b) Central: Onset is gradual; no associated auditory symptoms; often presents with other neurologic signs and symptoms like ataxia, dysarthria, dysphagia, focal or lateralized weakness 1) Etiologies a) Brainstem ischemia b) Multiple sclerosis c) Veistibular migraine b. Symptoms and Signs (1) Vertigo is the cardinal symptoms of vestibular disease. (a) Vertigo is typically experienced as a distinct “spinning” sensation or a sense of tumbling or of falling forward or backward. (2) It should be distinguished from imbalance, light-headedness, and syncope, all of which are non-vestibular in origin. (3) Nausea and vomiting are typical with acute vertigo c. Evaluation (1) A thorough history will often narrow down, if not confirm the diagnosis. (2) Critical elements of the history include the duration of the discrete vertiginous episodes (seconds, minutes to hours, or days), and associated symptoms. (3) The physical examination of the patient with vertigo includes evaluation of the ears, observation of eye motion and nystagmus in response to head turning, cranial nerve examination, and Romberg testing. (4) In acute peripheral lesions, nystagmus is usually horizontal with a rotatory component; the fast phase usually beats away from the diseased side. (5) Visual fixation tends to inhibit nystagmus except in very acute peripheral lesions or with CNS disease. (6) In benign paroxysmal positioning vertigo, Dix-Hallpike testing (quickly lowering the patient to the supine position with the head extending over the edge and placed 30 degrees lower than the body, turned either to the left or right) will elicit a delayed onset (~10 sec) fatigable nystagmus. (7) Non-fatigable nystagmus in this position indicates CNS disease. d. Causes (1) Peripheral vestibulopathy usually causes vertigo of sudden onset, may be so severe that the patient is unable to walk or stand, and is frequently accompanied by nausea and vomiting. (a) Tinnitus and hearing loss may be associated and provide strong support for a peripheral (i.e., otologic) origin. (2) Central disease (a) In contrast to peripheral forms of vertigo, dizziness arising from CNS disease tends to develop gradually and then becomes progressively more severe and debilitating. (b) Nystagmus is not always present but can occur in any direction and may be dissociated in the two eyes. (c) The associated nystagmus is often non- fatigable, vertical rather than horizontal in orientation, without latency, and unsuppressed by visual fixation. (d) Evaluation of central audio vestibular dysfunction requires MRI of the brain. (e) Episodic vertigo can occur in patients with diplopia from external ophthalmoplegia and is maximal when the patient looks in the direction where the separation of images is greatest. (f) Cerebral lesions involving the temporal cortex may also produce vertigo; it is sometimes the initial symptom of a seizure. (g) Finally, vertigo may be a feature of a number of systemic disorders and can occur as a side effect of certain anticonvulsant, antibiotic, hypnotic, analgesic, and tranquilizer medications or of alcohol. e. Workup (1) Laboratory investigations, such as audiologic evaluation, caloric stimulation, ENG, VNG, vestibular-evoked myogenic potentials (VEMPs), and MRI, are indicated in patients with persistent vertigo or when CNS disease is suspected. (2) These studies help distinguish between central and peripheral lesions and identify causes requiring specific therapy. f. Treatment (1) Vertigo treatment can be divided into three categories: those specific to the underlying vestibular disease, those aimed at the symptom of vertigo, and those aimed at promoting recovery. (2) Medications to suppress vestibular symptoms are best used for alleviating acute episodes that last at least a few hours or days and are not as useful for brief episodes (Benign Paroxysmal Positional Vertigo), unless they occur with high frequency. Doses should be started low and increased to positive effect or side effect. (3) Recommend starting with low dose and increase to positive effect or side effect and stopping within 48 hours if the patient's symptoms allow. (a) Meclizine (Antivert) - 1st generation antihistamine 1) Dose: 25 to 50mg q 6-12 hours PRN dizziness 2) MOA: Suppresses vestibular end-organ receptors and inhibits activation of central cholinergic pathways 3) Adverse Reactions: Drowsiness, fatigue, headache, vomiting, xerostomia, anaphylactoic reaction, blurred vision 4) Contraindications: hypersensitivity to the drug 5) Note: May cause CNS depression, which may impair physical or mental abilities; patients must be cautioned about performing tasks which require mental alertness (operating machinery, driving) (b) Diazepam (Valium) - Anticonvulsant, Benzodiazepine 1) Dosing: 1 mg PO q 12 hours as needed for dizziness 2) MOA: Binds to benzodiazepine receptors; enhances GABA effects 3) Adverse Reactions: Respiratory depression, suicidality, syncope, drowsiness, ataxia, depression, confusion 4) Contraindications: Renal impairment, hepatic impairment, CNS depression, depression, respiratory depression (c) Ondansetron (Zofran) – antiemetic 1) Dose: 4mg PO/IV q8 hours as needed 2) MOA: Selectively antagonizes serotonin 5-HT3 receptors 3) Adverse Reactions: QT prolongation, Stevens- Johnson Syndrome, serotonin syndrome, HA, diarrhea, agitation, pruritus 4) Contraindications: Ventricular arrhythmias, recent MI, CHF, hepatic impairment. (d) Promethazine (Phenergan) - 1st generation antihistamine, anti- nausea and vomiting medication 1) Dose: 12.5 - 25mg PO/IM/IV/Rectal every 4-6 hours as needed 2) MOA: Non-selectively antagonizes central and peripheral histamine H1 receptors; possesses anticholinergic properties, resulting in antiemetic and sedative effects 3) Adverse Reactions: Respiratory depression, seizures, hallucinations, heat stroke, drowsiness, sedation, photosensitivity 4) Contraindications: Comatose patients, respiratory depression, elderly patients, seizure disorder, asthma (e) Recommend vestibular exercises in patients with peripheral vestibular disorders to promote early recovery. Vestibular rehabilitation may be accomplished by a series of sessions with a physical therapist, or the patient may be trained to do these independently, at home. Most patients with vertigo prefer to lie with their head still but vestibular rehabilitation forces them to perform challenging balance exercises with several potential benefits.

CLINICAL CARE OF THE NERVOUS SYSTEM Flashcards

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