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Neurological Problems Bell’s Palsy: Description Idiopathic paralysis of CN VII Most common cause of facial paralysis Increased incidence in ages 30-40 and >70 At increased risk: DM, HTN, lipid problems Bell’s Palsy: Clinical Presentation Acute onset; peaks within hours Etiology of lesion is unclear, but causes anoxia and swelling of the facial nerve Symptoms usually unilateral Symptoms vary depending on level of lesion that is preventing transmission of nerve impulses down the facial nerve Involves innervation of forehead, eye, mouth Bell’s Palsy: Symptoms Inability to close the eye Eye pain pain and tearing Drooling Hyperacusis (sound distortion), tinnitus, ear pain Fever Loss of taste Bell’s Palsy: History Onset, evolution, presentation of symptoms Effect of symptoms on day-to-day functioning Control of DM, HTN, hyperlipidemia Recent herpes zoster infection May be ear involvement Ramsey Hunt syndrome (vesicles on TM) Physical Exam for Bell’s Palsy What will you include? Diagnostic Studies for Bell’s Palsy CBC with diff ESR Serum cholesterol and triglycerides FBS (Hgb A1c if known diabetic) Tonogram Lyme titer Electromyography (EMG) What are you looking for? Infectious etiologies (OM, herpes zoster, Lyme disease) Neoplastic lesions (acoustic neuromas, parotid tumors) Other neuro causes (CBA, Guillain-Barre syndrome Trauma Clinical Management Most will recover either totally or to an acceptable degree Increasing age is a risk factor for a less-than-complete recovery. Pharmacologic Measures To prevent corneal injury: methylcellulose drops Best results if started within 3 days of symptom onset Corticosteroids 60 mg days 1 through 3 then taper by 10 mg/d for 6 days Use cautiously with diabetics Nonpharmacologic Measures Patch or tape down affected eye at night Electromyography stimulation Controversial: facial nerve decompression Facial nerve graft Nerve anastomosis Tic Douloureux (also known as: Trigeminal (CN V) Neuralgia Etiology: thought to be related to compression of trigeminal nerve, perhaps from vascular loop Other causes: benign tumors (meningioma, acoustic neuroma plaque formation in multiple sclerosis Symptoms Intense, stabbing pain within distribution of trigeminal nerve May begin spontaneously or with facial movements such as speaking, chewing Range: 1-2 attacks/day to 10-20/hour More pronounced during day Trigger points: touching of the face wind blowing across the face hot or cold liquids Usually unilateral Involves 2nd or 3rd division of trigeminal; rarely ophthalmic division Majority > age 50 Women > men Treatment Pain relief: anticonvulsant meds carbamazepine (Tegretol) - 80% effective initial dose: 200 mg/day increase slowly (100-200 mg every 2-3 days) Check CBC and LFTs periodically phenytoin (Dilantin) - 50% effective Surgical therapy percutaneous trigeminal neurolysis microvascular decompression Herpes Zoster (Alias: Shingles) Epidemiology Incidence rises with increasing age Nearly 70% occur in people > age 50 About 20% of general population will experience zoster Approximately 50% of people who live beyond age 80 can expect to have zoster No difference in gender, race, or season Etiology Acute varicella infection, usually as child Latent virus takes up residency in the sensory nerve ganglia Periodically reverts to infectious state, but held at bay by immune functions (= contained reversion) As immune function declines, host resistance drops,”contained” reversion eventually breaks through to cause herpes zoster Clinical Presentation Usually heralded by dermatomal pain, sometimes accompanied by malaise, fever Pain precedes vesicular eruption by 2-3 days Reports of 2 weeks, 100 days Within few days: skin overlying the dermatome reddens and blisters A few vesicles are usually grouped on one erythematous base (vs. scattered, single vesicles of chickenpox) Several days later: vesicles become pustular and develop crusts. Thoracic dermatomes most often affected Scabs form. *At this point, the lesions no longer contain virus May affect > 1 dermatome Early Diagnosis Important Prompt recognition of herpes zoster infection is important because antiviral therapy, when appropriate, is maximally effective only when started during the earliest stages of the eruption Course of herpes zoster Depends on patient’s age, immune status New lesions continue to appear for 2-3 days Lesions usually crust/scab within 14 days Pain may linger for several more days The older the patient, the longer the duration of zoster-associated pain Elderly: greatest risk of postherpetic neuralgia Diagnosis Usually clinical dx. without lab tests Tricky: herpes simplex vs. herpes zoster HSV may mimic zoster, esp. when on thighs, buttocks, or face Frequent recurrences = hallmark of HSV Consider this first when an immunocompetent patient reports repeated outbreaks of herpetic lesions Lesions of sacrum: sacral zoster vs. anal HSV If unsure: viral antigen assays Can It Recur? < 5% of immunocompetent patients who have 1 episode of herpes zoster will have another; if so, usually separated by years This may change as we live longer 50% of recurrent zoster in immunocompetent adults develops in same dermatome as pervious outbreaks Subsequent episodes may be more painful, possibly because the patient is older Ramsey Hunt syndrome Facial paralysis that resembles Bell’s palsy Small herpetic vesicles on external surface of ear, auditory canal, TM, hard palate Zoster skin lesions are not prominent because the facial nerve has little cutaneous distribution Ophthalmic involvement 15% have involvement in the ophthalmic distribution of the trigeminal nerve Hutchinson’s sign: lesion on the tip of the nose Tip-off to corneal involvement and associated keratitis Can have eye involved without Hutchinson’s Ophthalmologist referral What Do You Think? Should herpes zoster in an apparently healthy young or middle-aged adult always trigger a search for HIV infection or occult malignancy? Treatment The sooner antiviral therapy is started, the more likely the benefit Critical period: 48-72 hrs. after onset of rash Antiviral therapy to reduce inflammation, relieve acute pain, prevent chronic pain, & prevent ophthalmic complications: 7 days Acyclovir (Zovirax): 800 mg q4h 5X/day Famciclovir (Famvir) 500-750 mg tid Valacyclovir (Valtrex) 1000 mg tid Treatment Some choose to co-administer low-dose corticosteroids to reduce inflammation and chance of postherpetic neuralgia Steroids, however, carry a risk for potentiating the infection as well as producing adverse effects Risk > benefits Postherpetic neuralgia (PHN) “The pain that lingers” Seen almost exclusively in elderly patients May persist weeks to months, even years May result from damage caused by virus to the sensory ganglia Treatment for PHN Topicals: capsaicin cream (Zostrix), Burrow’s solution, calamine lotion, ethyl chloride spray, lidocaine/prilocaine cream Systemic: tricyclic antidepressants (Elavil), anticonvulsants (Tegretol), antivirals (Zovirax) Other: TENS, lidocaine injection, nerve block injections, nerve resectioning Temporal Arteritis When an elderly person develops a H/A, it is important to test for temporal arteritis. Rare in persons under 60 years old Also known as giant cell arteritis A vasculitic disorder of the cranial arteries Produces temporal H/A Clinical Presentation Headache Local tenderness to palpation of the forehead and temporal arteries Possibly visual loss Systemic c/o weight loss, anorexia, weakness, and low-grade fever may precede H/A Assessment/Diagnostic Studies ESR elevated Increased serum globulins Diagnosis is confirmed by a temporal artery biopsy Temporal artery biopsy shows distinctive inflammatory changes Clinical Management Immediate initiation of high-dose steroid treatment Medical emergency: ischemia may cause blindness due to retinal infarct, Many episode-free after 1-2 years of treatment relieves H/A and systemic sx. normalizes ESR in about 4 weeks MI, CVA Cerebrovascular Accident (Stroke) One of the most common neurologic problems in the elderly Definitions Stroke = a rapidly developing vascular deficit in the brain, which causes a focal disturbance of brain function for > 24 hours Transient Ischemic Attack (TIA) = a focal deficit of vascular origin that resolves in < 24 hours Reversible ischemic neurologic deficit (RIND) = a focal deficit of vascular origin which last longer than 24 hours, but resolves completely TIAs Often due to platelet emboli from the heart 25-40% of patients who have had TIAs go on to have a major cerebrovascular accident (CVA) Stroke 3rd most common cause of death in industrialized countries 30% of stroke survivors have obvious neurologic deficits but are able to live an independent life 20% die within 1 month of CVA 50% of stroke survivors have significant, permanent disabilities that require them to have assistance and supervision CVAs 70% occur in person over 65 years old HTN is contributing factor in 70% of CVAs DM doubles the risk of CVAs Other risk factors of CVA Cardiac disease atrial fib valvular heart disease cardiac failure ischemic heart disease atherosclerotic vascular disease Oral contraceptives Severe anemias Hypotension (particularly in the elderly) 2 major causes of CVAs (1) hemorrhages due to hematomas and aneurysms that bleed into the brain (2) ischemia due to thrombosis and embolism in which a lack of blood to an area of the brain causes lack of oxygenation and destruction of the brain tissue Constraint-Induced Movement Therapy (CI Therapy) The Patient with a TIA What do you do re: - assessment/diagnosis? - treatment? Acute Stroke Management Labs: CBC, lytes, CMP, PT, PTT, U/A, EKG CXR CT Scan: most useful to establish if stroke is ischemic or hemorrhagic event Hemorrhagic stroke appears immediately as area of increased density Ischemic stroke may not cause a visible abnormality on CT scan for 2-4 days after onset of symptoms MRI: more sensitive if brain stem, cerebellum lesion suspected BP Management in CVA Often BP rises dramatically as attempt to maintain adequate cerebral perfusion 2/3 with HTN at time of stroke become normotensive without any intervention in a few days after acute event Sublingual CCB’s should not be given, since sudden/rapid decline in BP may increase the volume of brain damage If hypotension is noted, hypovolemia is most likely cause Dizziness Most common complaint among persons age 75 and older Statistics Although 80% of patients suffering from dizziness reported the symptom to the primary care provider, only 56% received treatment. Of those treated, 90% received a prescription for meclizine. Definitions: Vertigo An illusion of movement, usually of rotation Arises from disturbance of the vestibular system Common causes: benign positional vertigo, neurolabyrinthitis, vascular disease, Meniere’s disease Definitions: Presyncopal lightheadedness Sensation that one is about to pass out Causes: rapid position change, lying in hot sun, excess alcohol intake Arises because cerebral cortex is temporarily not receiving adequate oxygen (diminished blood flow) In elderly: vasovagal episodes, medication, cardiac dysrhythmia Definitions: Dysequilibrium Sense of imbalance (body sensation more than a head sensation) Arises from disruption of any structures of the balance system In elderly: multifactorial - poor vision from cataracts, hip weakness from arthritis, cerebral impairment due to meds Definitions: Vague, difficult -to-categorize dizziness Often accompanies psychological conditions such as anxiety and depression Common associate somatic complaints: H/A, “nerves”, neck pain, insomnia, weakness, fatigue Check for hyperventilation Due to biochemical changes in the brain triggered by stress or emotional states Physical Examination Postural BP measurement drop of systolic of 20+, diastolic drop of 10+, or both Forced hyperventilation (when anxiety is possible diagnosis) Hallpike maneuver Marching in place with eyes closed (checks for unilateral vestibular dysfunction) Management Benign positional vertigo (BPV) Medication generally not helpful Physical exercises Presyncope Usually due to postural hypotension “Say a little prayer” Other causes: acute stress, blood drawing and other procedures, urination (micturition syncope), cardiac dysrhythmias Meclizine, dimenhydrinate, and other antihistamines provide relief for acute peripheral vestibular problems such as labyrinthitis or attacks of Meniere’s disease For labyrinthitis, may also need compazine for N&V Parkinson’s Disease An idiopathic degenerative process of the pigmented dopaminergic neurons of the substantia nigra Affects 1% of all persons over age 50 Clinical Presentation Decreased voluntary movement Reactive depression common as disabilities increase Increased involuntary movements Impaired muscle tone Impaired postural reflexes Initially, symptoms are unilateral, but within 1-2 years, progress to become bilateral Changes on Physical Exam Rigidity with cogwheeling: increased tone with rachetlike sensation Retropulsion: steps or falls backwards if gently pushed (unable to resist the push and stay in place) Intention tremor (when attempting to complete a task) Festinant gait: uneven, shuffling gait that chanages from walking to running pace or may freeze and stop Resting tremor Pill rolling (characteristic of PD) Bradykinesia (slowed voluntary muscle movement that deteriorates with repetition; may cause client to freeze (blank facial expression, drooling, etc.) Poor postural reflexes (bends forward, with poor balance and slow adjustment, contributing to falls; difficulty changing direction while walking) Mental status changes Weight loss Contractures Seborrheic dermatitis (eyebrows, ears, scalp line) Stages of Parkinson’s Stage I Unilateral involvement Tremors of upper extremities Milk rigidity Uneven gait (affected arm in flexed position; posture leaning toward unaffected side) Blank facial expression Stage II Bilateral involvement Slow, shuffling gait, with stooped position Slowing of all movements (bradykinesia) Stage III Postural instability with tendency to fall Retropulsion and propulsion Assistance with ADLs becomes necessary Stage IV Rigidity and bradykinesia become disabling, requiring substantial assistance with ADLs Standing is unstable, falls are frequent Retropulsion and propulsion become severe Use of wheelchair becomes necessary Stage V: Bradykinesia and rigidity become severe, leaving the person unable to move Facial expression becomes fixed and staring Speech becomes difficult to understand Difficulty swallowing Total assistance required with all ADL and movement Walking is no longer possible Management Goal: replenishing the dopamine stores in the brain Dopamine cannot cross blood-brain barrier -administer levodopa (metabolic precursor) -attempt to stimulate release of dopamine from the substantia nigra Pharmacologic Measures Amantadine (Symmetrel) resembles anticholinergic drugs often first med used for treatment releases dopamine from the cells of substantia nigra decreases rigidity, tremors, bradykinesia effective in 50% of patients 100 mg po twice a day SE: skin discoloration, feet swelling, confusion,delusions, hallucinations Levodopa-carbidopa (Sinemet) and levodopa-benserazide (Madopar) block the peripheral decarboxylation of levodopa, therefore slowing its conversion to dopamine in extracerebral tissues. Allows increased availability of dopamine in the brain Response may decrease over time, requiring a higher dose to achieve effect Use delayed until sx. impact quality of life Mirapex and Requip Anticholinergics Nonergot dopamine receptor agonists High affinity for dopamine D2 receptors Cogentin, Artane, Akineton anticholinergics block action of acetylcholine, which may decrease rigidity and tremors may prolong dopamine effects by blocking dopamine reuptake and storage SE: dry mouth, blurred vision, constipation, difficulty voiding, mental status changes Pharmacologic Measures Bromocriptine (Parlodel) and Pergolide (Permar) dopamine receptor antagonists adjunct to Sinement(when used in combo, less Sinemet may be used to get sx. Control) mimic effects of dopamine SE: nausea, dizziness, mental status changes Eldepryl (selegiline hydrochloride) monoamine oxidase inhibitor adjunct to or prior to beginning Sinemet may directly increase dopaminergic activity by decreasing uptake of dopamine into the nerve cells 5 mg po twice a day, with breakfast and lunch Nonpharmacologic Measures No care; treatment is symptomatic PT and OT Speech therapy: swallowing, drooling Dietician Home care National organizations; support groups Reflex Sympathetic Dystrophy Syndrome http://www.ninds.nih.gov/patients/DISORDER/rsds/rsds.htm What is RSDS? Chronic condition characterized by Severe burning pain Pathological changes in bone and skin Excessive sweating Tissue swelling Extreme sensitivity to touch A nerve disorder that usually occurs at the site of an injury RSDS Pain reported is out of proportion to the severity of the injury and gets worse, rather than better, over time Initially localized, but spreads over time, often involving an entire limb (and possibly the opposite extremity as well) Pain is continuous and may be heightened by emotional stress One visible sign of RSDS near the site of injury is warm, shiny red skin that later becomes cool and bluish Cause unknown: thought to be result of damaged nerves of the SNS Moving or touching the limb is often intolerable Eventually the joints become stiff from disuse and the skin, muscle, and bone atrophy More common between ages 40-60 Most frequently seen in women 2-5% of those with peripheral nerve injury and 12-21% of those with hemiplegia will suffer from RSDS Treatment Corticosteroids, vasodilators, alpha or beta-adrenergic blocking compounds Elevation of extremity PT Injection of a local anesthetic (lidocaine) usually 1st step in treatment TENS Surgical or chemical sympathectomy Multiple Sclerosis Etiology: Theories Autoimmune disease directed against myelin proteins, oligodendroglia cells, or other antigens Chronic infection of the central nervous system Environmental (increased incidence as distance from equator increases) Genetics (90-95% white, family trend, F:M3:1) Key Symptoms Neurologic symptoms lasting days to weeks in a young adult Numbness, weakness, and ataxia, often appearing together Monocular visual blurring or binocular diplopia Worsening symptoms with vigorous activity or heat Bowel, bladder, and sexual dysfunction Key Signs Signs often bilateral Ataxia or abnormal gait Weakness in an upper motor neuron pattern (asymmetrical weakness most often of the legs) Internuclear ophthalmoplegia (paralysis of ocular motor nerves) Diminished visual acuity Diagnosis MRI: relatively specific, but false +/CSF: <40 WBCs, predominantly lymphocytes, protein usually normal, oligoclonal immunoglobulin bands (+ CSF, - serum), IgG index > 0.70 (CFS/Serum) Diagnosis Diagnosed only when physiologically consistent symptoms and signs and laboratory tests converge to suggestion involvement of white matter projects from multiple areas within the CNS. S/Sx fluctuate with time. No other pathology can exist to explain the complaints and findings. Treatment Symptomatic treatment for fatigue, depression, spasticity, urgency, constipation, neuralogic pain, chronic aching pains, postural tremor Disease exacerbations: methylprednisolone IV, ACTH IV or IM PT/OT Treatment palliative; course unpredictable
