Exam 3 Neuro Flashcards

Question

When a patient has red flag findings like Combo of fever, wt loss, visual changes, jaw claudication, temporal artery tenderness, and proximal myalgias what are the possible causes of the headache?

Answer 1

Giant cell arteritis

Answer 2

Idiopathic intracranial HTN

Answer 3

A simple analgesic, such as ASA, Acetaminophen, Ibuprofen, or naproxen, taken immediately, may abort the HA Erogotamines- Cafergot PO & Dihydroegotamine mesylaste (DHE 45) IV (abort thp.) Triptans- Sumatriptan, zolmitriptan, naratriptan, rizatriptan...etc (abortive therapy) Prochlorperazine rectal, PO, IV, IM Butalbital combo- risk overuse and abuse- last resort!

Answer 4

They can cause rebound HA and addiction

Answer 5

Neuromodulation-Transcranial magnetic stimulation was effective in aborting migraine with aura- but costly. Diet counseling (avoid triggers) Lifestyle modification (wt loss, smoking cessation, and nutritional diet) shown to decrease episodes During attacks, pt should stay in a dark, quiet environment and rest Warm baths may help pt to relax

Answer 6

Avoid triggers, regular sleep, meals, and hydration, HA diary for triggers B-blockers: Propranolol ,Metoprolol Candesartan, guanfacine, & verapamil Antiepileptics:Valproic acid ,Topiramate Antidepressants:Amitriptyline ,venlafaxine Onabotulinumtoxin A(Botox)- dose dependent on location Riboflavin

Answer 7

Acetaminophen ASA NSAIDs (ibuprofen, ketoprofen, and naproxen) more effective than acetomen. Ketorolac IM is effective for in-office or inpatient

Answer 8

Heat, ice, massage of neck and temples, rest and relaxation techniques, exercise, and regular sleep. F/U in 2wks to monitor progress Behavioral therapies- tx comorbid anxiety or depression!!

Answer 9

Acute attack: Sumatriptan (Imitrex), Zolmitriptan, DHE 45, Ergotamine tartrate aerosol, 100% OX inhalation - 7L/min for 15 min Avoid medication oversue!! = analgesic rebound HA

Answer 10

Lifestyle modification and supportive care- limited benefit d/t unknown precipitating factors Avoid triggers if known F/U visits at regular intervals

Answer 11

Verapamil, 240-480 mg/day Lithium carbonate, 150-600mg/day Topiramate, 50-200 mg/day Valproic acid 500-2000 mg/da

Answer 12

Blindness or visual disturbances throughout both visual fields are initially accompanied or followed by dysarthria, dysequilibrium, tinnitus, and perioral and distal paresthesias and are sometimes followed by transient loss or impairment of consciousness or by a confusional state. This, in turn, is followed by a throbbing (usually occipital) headache, often with nausea and vomiting

Answer 13

lateralized pain—often about the eye—is accompanied by nausea, vomiting, and diplopia due to transient external ophthalmoplegia. The ophthalmoplegia is due to third nerve palsy, sometimes with accompanying sixth nerve involvement, and may outlast the orbital pain by several days or even weeks. The ophthalmic division of the fifth nerve has also been affected in some patients. Ophthalmoplegic migraine is rare and a diagnosis of exclusion; more common causes of a painful ophthalmoplegia are internal carotid artery aneurysms and diabetes.

Answer 14

Emotions- anticipation, anxiety, depression, excitement, frustration, stress Food Ingredients- aspartame (diet sodas & artificial sweeteners), monosodium glutamate (chinese food and canned soups), nitrates (cured meats), phenylethylamine (chocolate), tyramine (aged cheeses and chianti wine), yellow food coloring Drugs- alcohol, analgesic (excessive or withdrawal), caffeine (excessive or withdrawal), cimetidine, cocaine, estrogen (oral contraceptives), nitroglycerin Other factors- carbon monoxide, hormonal changes in women, flickering lights or glare, loud noises, hypoglycemia, change in altitude or barometric pressure, altered sleep pattern (over or under)

Answer 15

Most symptoms don’t develop until tumor is well advanced. Progressive neurological deficits HA Seizures Other symptoms include Hydrocephalus, dysphagia, confusion, lethargy, vision changes, endocrine disturbances

Answer 16

Can be primary malignancy or secondary (common metastatic sources) Lung, melanoma, renal, and breast, GI tract

Answer 17

Treat with an osmotic diuretic, Mannitol (Osmitrol) 0.25-2 grams/kg of a 20% solutions IV for 3-5 minutes ***Avoid LP in a patient with ICP***

Answer 18

The agent of choice for recurrent seizure caused by tumors/edema is phenytoin (Dilantin) 1 gm IV or PO as a loading dose, followed by 300 mg/day in divided doses as a maintenance dose. Levetiracetam (Keppra) starting at 500 mg IV or PO BID (Barkley p. 29)

Answer 19

Headache the most common and worst symptom, usually dull, constant and worse at night. Seizures are also a common symptom, usually seen in mets, type of seizure depends on the size and location of the tumor. Focal neurologic s/s like muscle weakness, sensory changes, or visual disturbances. Memory changes, personality changes may also be seen

Answer 20

Progressive intellectual decline, slowing mental activity, personality changes, contralateral grasp reflexes, expressive aphasia

Answer 21

Seizures, olfactory or gustatory hallucinations. Smacking or licking lips, emotional changes, behavioral changes, visual disturbances.

Answer 22

Contralateral disturbances of sensation, sensory loss, inattention, or a combination of these. Astereognosis, the ability to differentiate between size, textures, weight and shape become impaired. Denial, left right confusion, dressing and constructional apraxia.

Answer 23

Cranial nerve palsies, ataxia, nystagmus, sensory deficits in the limbs, and incoordination

Answer 24

MRI is the procedure of choice for all brain tumor types, because of its high sensitivity, capacity to delineate small tumors in sites near bone, sensitivity to tissue edema, and inherent multiplanar capability that allows a n accurate localization of tumor and their relation to normal structure CT can be performed but is less helpful for smaller tumors

Answer 25

Glioblastoma multiforme is the most common primary tumor, followed by meningioma and astrocytoma

Answer 26

Total surgical removal is usually not possible and there is poor response to radiation. Brachytherapy may have positive effects on survival. Brachytherapy is the stereotactic implantation of interstitial radionuclide sources (Barkley p. 29). Other noninvasive treatments that have had success are: Gamma knife Proton beam Modified linear accelerator (used with stereotactic guidance) Combined modality therapy with surgery, radiation treatment, and chemotherapy has improved survival rate in GBM. Symptomatic treatment includes corticosteroids to reduce cerebral edema, antiepileptic drugs for seizures, and painkillers for HA

Answer 27

an acquired, persistent, & progressive impairment in intellectual function with compromise of memory and at least one other cognitive domain like: Aphasia (difficulty word finding), (left parietal lobe). Apraxia (inability to perform motor tasks eg cutting a loaf of bread despite intact motor function), Agnosia ( inability to recognize objects) Or impaired executive fcn (planning, judgement, mental flexibility).

Answer 28

results from irreversible neuronal damage that cannot be cured. The histopathology is characterized by neuritic plaques, neurofibrillary tangles, & degeneration of cholinergic neurons in the hippocampus and cerebral cortex. 𝛃-amyloid is present in high levels which may contribute to neuronal injury. AD results in cerebral atrophy.

Answer 29

Nerve cell disease e.g alzheimer's, parkinson's, huntington’s Vascular - multi infarct dementia, stroke, arteritis Infections - HIV, syphilis, meningitis, abscess, encephalitis, creutz jakob disease CNS anoxia e.g in overdose, cardiac arrest nutritional deficits - vitamin B!@, folate deficiency, Toxic reaction - chronic etoh use/abuse, drug toxicity Subdural hematoma Hydrocephalus Chronic seizures Lewy body dementia Other illnesses eg kidney, liver, CHF, hypoxia, arrhythmias, MI, hypo/hyperthyroidism

Answer 30

Mini Mental State Exam (MMSE) Mini-cog - is a 3 item test completed in < 3 minutes ( repeat 3 items then draw a clock) if pt recalls all 3 items after 3 minutes then the test is normal. If pt recalls 0 items test is abnormal and don't score the clock. If pt fails this test then further cognitive evaluation is warranted. The montreal cognitive assessment - 30 point test that examines several areas of cognitive function. Highly sensitive for dementia. Addenbrooke's’ Cognitive Examination - Revised

Answer 31

The cognitive disturbance is of insidious onset and is progressive, based on evidence from the history or serial cognitive examination The presence of at least two of the following: Parkinsonism (rigidity, resting tremor, bradykinesia, postural instability, parkinsonian gait disorder) Prominent, fully formed visual hallucinations Substantial fluctuations in alertness or cognition Rapid eye movement sleep behavior disorder Severe worsening of parkinsonism by antipsychotic drugs The disturbance is not accounted for by a systemic disease or another brain disease

Answer 32

Memory probs - short term memory loss ( unable to recall recent events or conversations, repetitive questioning Visuospatial abilities (becoming lost in familiar surroundings, poor navigation) Personality changes - mood changes, apathy(lack of emotion) then psychosis and agitation in later stages Behavioral difficulties (wandering, inappropriate sexual behavior, & aggression) may worsen as disease progresses. Hallucinations, delusions, depression often occur as dementia worsens End stage dementia - near mutism, inability to sit up, hold up the head, inability to track objects with eyes, eat, swallow, weight loss, bowel/bladder incontinence, recurrent resp and urinary infections.

Answer 33

present with psychomotor slowing, reduced attention, early loss of executive function, & personality changes.

Answer 34

fluctuating cognitive impairment , rigidity, bradykinesia are the primary signs. These pts often have visual hallucinations - typically of people & animals.

Answer 35

includes pick disease. Pts manifest with personality changes (euphoria, disinhibition, apathy, & compulsive behaviors.

Answer 36

CBC, BMP, calcium, BUN, creatinine, glucose, TSH, & vitamin B12 levels, VDRL, HIV, ABG’s, UA with culture, albumin, alcohol level, and check for illicit drugs in (UDS).Lumbar puncture ( r/o meningitis), EEG (if there is seizures)

Answer 37

Safety - esp. if wandering , impaired driving, leaving stove unattended, and address accidents with patient and family Address hoarding, hiding objects, repetttive questioning, withdrawal, sexual innapropriate behavior which respond to behavioral therapies.

Answer 38

Acetylcholinesterase Inhibitors eg donepezil, galantamine, rivastigmine for mild to moderate alzheimer's. These meds may also have benefit in pts with vascular dementia or dementia with lewy bodies. S/E n/d, anorexia, weight loss, & syncope Memantine - specifically beneficial for pts with advanced disease Symptomatic mgmt of depression, agitation, delusions, hallucinations which may respond to specific medications

Answer 39

Sleep hygiene - use the bed for sleep only, awake at same time everyday, & establish a bedtime routine Stop nicotine /caffeine Alcohol cessation Establish a daily exercise regimen Alcohol cessation

Answer 40

Lorazepam - short term use only 1-2 wks Zolpidem Temazepam Antihistamines eg benadryl & hydroxyzine Atypical antidepressant trazodone ( adv. not habit forming esp. in lower doses)

Answer 41

Central nervous system disease Systemic disease Interaction effects of withdrawal or intoxication from drugs or toxic agents (such as mercury or heavy metals) Age – young children and those older than 60 years Preexisting brain damage or dementia History of alcoholism Diabetes Malnutrition Cancer 30% of ICU patients develop delirium

Answer 42

D – drugs E – electrolyte and physiologic abnormalities L – lack of drugs (withdrawal) I – infection R – reduced sensory input (blindness, deafness) I – intracranial problems (CVA, meningitis, seizure) U – urinary retention and fecal impaction M – myocardial problems (MI, arrhythmias, CHF)

Answer 43

Sudden; days or weeks. Associated with a physical stressor

Answer 44

Gradual; months or years

Answer 45

Clouded sensorium, irritability and anxiety, misperception of sensory stimuli, possible hallucinations, lucid periods, alternating with confusion, suspiciousness, agitation

Answer 46

Memory loss, decreased intellectual functioning (confabulation and circumstantiality), loss of executive function

Answer 47

Toxins, alcohol/drug abuse, CNS or cardiac infarction, hypoxia, head trauma, adverse effects of medications, infections, electrolyte imbalance, poor nutrition, anesthesia, tumors, endocrine problems, impactions in the elderly

Answer 48

Neurotransmitter deficit, cortical atrophy, ventricular dilation, cerebrovascular accident (multi-infarct dementia), Lewy bodies, Alzheimer’s disease, Parkinson’s disease, Huntington’s chorea

Answer 49

Usually older than 60

Answer 50

Confusion Assessment Method – bedside instrument for the assessment of delirium - available as Long CAM, Short CAM, and 3D (3-minute diagnostic) CAM. 1 – acute onset and fluctuating course AND 2 – inattention and EITHER 3 – disorganized thinking OR 4 – altered level of consciousness = CAM positive for delirium

Answer 51

Kidney or liver failure Thyroid, adrenal, or glucose dysregulation Anemia Vitamin deficiency – Wernicke’s encephalopathy or Vitamin B12 deficiency Inborn metabolic errors – porphyrias or Wilson’s disease

Answer 52

Antipsychotics agents (such as haloperidol or quetiapine) are medications of choice. Dexmedetomidine or propofol (or both) may be useful for ventilated patients in the ICU

Answer 53

90% of all pts with GCA have ESRs higher than 50mm/h. With it more often being more than 100. CRP can also be sensitive to GCA Temporal artery Biopsy Most pts also have a mild normochromic, normocytic anemia and thrombocytosis Alkaline phosphate (liver source) is elevated in 20% of pts with GCA

Answer 54

Temporal artery biopsy

Answer 55

Headache, scalp tenderness, visual symptoms (amaurosis fugax or diplopia), jaw claudication, or throat pain. Jaw pain is the highest predictive value. The temporal artery is usually normal on PE but may be nodular, enlarged, tender, or pulseless. Blindness usually results from the syndrome of anterior ischemic optic neuropathy, caused by occlusive arteritis of the posterior ciliary branch of the opthalmic artery. May produce no fundoscopic findings for the first 24-48 hours after the onset of blindness Can cause large vessel involvement. Asymmetry of pulses in the arms, murmur of aortic regurgitation, or bruits heard near the clavicle resulting from subclavian artery stenosis identify patient in who GCA has affected the aorta or major branches. Can cause high fever for pts over 65. Often the cause of fever or unknown origin Can complain of vague pain of nose, tongue, or ears

Answer 56

The urgency of early diagnosis and treatment in giant cell arteritis relates to the prevention of blindness. Once blindness develops, it is usually permanent. Prednisone (60 mg/day orally) should be initiated immediately and a temporal artery biopsy performed promptly thereafter. low-dose aspirin (~81 mg/day orally) may reduce the chance of visual loss or stroke

Answer 57

inflammatory infiltrate in the media and adventitia with lymphocytes, histiocytes, plasma cells, and giant cells

Answer 58

characterized by confusion, ataxia, and nystagmus leading to ophthalmoplegia (lateral rectus muscle weakness, conjugate gaze palsies); peripheral neuropathy may also be present.

Answer 59

It is due to thiamine deficiency and in the United States occurs most commonly in patients with alcoholism. It may also occur in patients with AIDS or hyperemesis gravidarum, and after bariatric surgery.

Answer 60

thiamine (100 mg) is given intravenously immediately and then intramuscularly on a daily basis until a satisfactory diet can be ensured after which the same dose is given orally. Some guidelines recommend initial doses of 200–500 mg intravenously three times daily for the first 5–7 days of treatment. Intravenous glucose given before thiamine may precipitate the syndrome or worsen the symptoms. The diagnosis is confirmed by the response in 1 or 2 days to treatment, which must not be delayed while awaiting laboratory confirmation of thiamine deficiency from a blood sample obtained prior to thiamine administration

Answer 61

Demyelinating disease of the central nervous system. Neurological symptoms caused by isolated inflammation, demyelination, and axonal damage leading to NERVE CONDUCTION DELAYS. Characterized by Relapses and Recovery.

Answer 62

Increased prevalence in populations living a greater distance from the equator Women has higher rate of incidence, earlier onset of disease in women Northern Europeans are more likely to develop MS Onset- AGE 20-40 No clear etiology, but thought to have multifactorial: Viral infection is precursor to exacerbation. No identified link to several proposed viruses

Answer 63

Most Common clear defined episodes of relapse and recovery (usual initial presentation)(82%)

Answer 64

-usually initiates with RR-MS followed by deterioration or progression of the disease. Patients usually do not return to baseline, few or no relapses

Answer 65

Continued disease progression, some plateaus and minor temporary improvements

Answer 66

progressive disease from onset with clear relapses. Continued progression of disease between relapses, occurs in 5% of MS patients

Answer 67

Rapid onset, progressive deterioration, disability and death in short period of time.

Answer 68

No deterioration after 10 years following onset of disease

Answer 69

Subjective Neurological Symptoms that last at least 24 hours resulting in increased disability Common initial presentation: weakness, numbness, tingling, unsteadiness, spastic paraparesis, retrobulbar optic neuritis diplopia (CMDT 1032) Motor weakness, spasticity, or stiffness, sensory alterations of numbness, tingling, burning or pain. Brain stem symptoms of double vision, dysarthria, dysphasia, dysphagia and vertigo. Visual defects, field defect decreased acuity, impaired color perception, and pain with eye movement. Cerebellar symptoms: gait ataxia, intention tremor and uncoordinated movement Cognitive Dysfunction: short-term memory, slowed processing, and difficulty with higher level problem solving. Fatigue presents in 90% of patients Sleep disorders, bladder bowel or sexual dysfunction, seizure, tonic spasms

Answer 70

Sensory Track disturbances, decreased vibratory sense, position sense, pinprick perception and temperature sensations. Reflex Alteration such as abnormal deep tendon reflexes, Positive babinskis sign, positive hoffmans sign, spastic limb weakness. Other signs: Nystamus, hearing loss, tinnitus, ataxia, lack of coordination, optic neuritis Initial symptom in 25% of patients), optic disk pallor, pupil defect, trigeminal neuralgia, emotional lability.

Answer 71

Test of choice, CSF Analysis Neurological Exam Multiple Foci best visualized by MRI

Answer 72

MRI-demonstrates white matter lesions in brain and spinal cord. T-2 Weighted lesions in periventricular white matter of brain “dawsons fingers” and spinal cord. Gadalinium enhancement and hypodensities (black holes) on T1 imaging. Cerebral atrophy present.

Answer 73

Consistent with MS if there is elevated IgG and oligoclonal bands in CSF, but not serum. Bands presents in 70% of MS positive patients, Presence indicates MS, absence does not rule out the disease

Answer 74

A definite diagnosis can never be based solely on lab findings. Should not be diagnosed unless there is evidence that two or more different regions of the central white matter have been affected at different times. Patients with a single event who do not satisfy criteria for MS may be diagnosed with clinically isolated syndrome (CIS)

Answer 75

Neurology Referral Mild acute exacerbations that do not produce functional decline may not require treatment. Glucocorticoids (500-1000 mg/day), oral or IV, usually IV methylprednisolone, duration is dependent on clinical response. Thought to promote early recovery but does not have long term effects. Short term pulse therapy preferred to prevent long term steroid effects. Disease Modification Medication: Initiate Early once diagnosis is established to reduce relapse, delay disability and reduces MRI lesion burden. Immunomodulators (Fingolimod, Betasron , Avenox, Rebif, Natalizumab) Immunosuppresent agents (Novantrone)

Answer 76

Dalfampriride- potassium channel blocker, approved to improve walking speed in pts with MS. Baclofen, tizanidine- Used to treat spasticity, Also Onobotulinum toxin for focal intractable spasticity Anti-cholinergicss can be used to treat urge incontinence. Treat Urinary retention with tamsulosin. Treat dysesthesias with gabapentin or pregamblin Fatigue- consider amantadine modafinil or stimulant Tremor- clonazepam, propranolol Depression and Anxiety Common -refer to both counselor and pysch.

Answer 77

Uhthoff's phenomenon or Uhthoff's sign is the temporary worsening of MS symptoms caused by an increase in temperature. It is usually applied to optic neuritis and other visual symptoms but can also refer to motor or sensory symptoms

Answer 78

Autoimmune attack on the acetylcholine receptor (AChR) complex at the postsynaptic membrane of the neuromuscular junction, decreasing normal motor transmission (Barkley p35). Also associated with HLA-DR3, HLA-B8, and HLA-DRB1 genes and those with muscle-specific tyrosine kinase (MuSK) antibodies can be included as well

Answer 79

Fluctuating weakness that worsens with physical activity; ptosis, diplopia, extraocular weakness, difficulty chewing or swallowing, facial weakness, and upper extremity muscle weakness. Deep tendon reflexes and sensation remain intact

Answer 80

Acetylcholine receptor antibodies, pts without these antibodies may have MuSK antibodies; · Tensilon test: cardiac monitoring and atropine must be available, a sudden brief improvement in muscle function occurs, helps differentiate between myasthenic and cholinergic crises, begin with 2mg IV and give additional 2mg q2m for a max dose of 10mg · repetitive nerve stimulation will show >10% decremental response after maximum contraction; · single fiber electrophysiology: increased “jitters” seen between 2 muscle fibers within the same motor unit, much more complicated and not widely available test · CT or MRI of anterior chest to look for thymoma or residual thymus tissue (chance of this increases with age)

Answer 81

acetylcholinesterase inhibitors: neostigmine or pyridostigmine (mestinon) dosed q4-6h, onset is 30m, monitor for cholinergic adverse effects (nausea, diarrhea, increased salivation, vomiting, cramps, increased bronchial secretions

Answer 82

Prednisone: inpatient (high dose initially and taper to minimum maintenance dose to prevent relapse) outpatient (gradually increase dose to effect) o Azathioprine o Other agent usually managed by specialist: cyclosporine, mycophenolate, and rituximab

Answer 83

Plasmapheresis or IVIG and protect airway

Answer 84

thymectomy; all MG pts <65 are good candidates and benefit from thymus removal unless weekness is restricted to extraocular muscles

Answer 85

beta-blockers, aminoglycoside and quinolone antibiotics, penicillamine, interferons, class I antiarrhythmics-procainamide, quinidine

Answer 86

FVC <15-20 ml/kg, max expiratory pressure <40cm h2o, neg inspiratory pressure <25-30 cm h2o, or weak cough effort in crisis

Answer 87

Exacerbation with respiratory involvement, requiring plasmapheresis can be managed on floor at most facilities

Answer 88

(ice bag and tensilon): Ice bag applied to eyes of pt with asymmetric ptosis will improve ptosis; tensilon described above, improvement should be seen in weakened muscle shortly after injection

Answer 89

variable weakness in proximal limb muscles that IMPROVES with activity; defective release of acetylcholine in response to nerve impulse causing power to steadily increase with sustained contraction; diagnosis with electrophysiology showing remarkably increase in motor response even in muscles not clinically weak, these pts often have undiagnosed small cell carcinoma

Answer 90

treatment with IVIG, plasmapheresis, prednisone, and azathioprine.

Answer 91

an acute, usually rapidly progressive, form of inflammatory demyelinating radiculoneuropathy; typically motor greater than sensory Characterized by a monophasic course of muscular weakness, mild distal sensory loss, and autonomic dysfunction, with the majority of patients reporting an antecedent infection. The maximum deficit is usually attained by week 4. Most frequently acquired demyelinating neuropathy.

Answer 92

Frequent antecedent infections include the following: upper respiratory infections, campylobacter jejuni enteritis, cytomegalovirus infection, epstein barr virus infection, hepatitis infection, HIV and mycoplasma infection

Answer 93

Usually symmetric, rapidly progressive distal muscle weakness and paresthesia, beginning in the legs and ascending rapidly to the arms, face, and oropharynx. Progression to total motor paralysis can ensue, leading to death from respiratory failure; therefore, this condition is considered a medical emergency. Deep tendon reflexes are often significantly reduced or absent on presentation, although this may take days to develop Weakness is more prominent than sensory signs and symptoms and may be more prominent proximally. Sensory involvement can present early, but usually without the objective signs of sensory dysfunction (ex. Stocking distribution sensory loss). Patient may have hyperesthesia, which may make the touch of a hand or a bed sheet very painful. Perception of joint position, vibration, and temperature may diminish. Bulbar involvement: bilateral facial and oropharyngeal paresis Difficulty swallowing (may have cranial nerve involvement) Urinary retention Respiratory paralysis (involvement of intercostal muscles) Autonomic dysfunction often present as hypersympathetic state with unexplained tachycardia, but may include bradycardia, BP fluctuations, inappropriate antidiuretic hormone secretion, cardiac arrhythmia and pupillary changes.

Answer 94

Most patients will have a good outcome without sequelae after appropriate treatment and management but approximately 5% will die from complications.

Answer 95

Respiratory insufficiency (caused by weakness of bulbar/intercostal muscle Mechanical ventilation may be needed if FVC is <12 to 15 ml/kg, vital capacity is rapidly decreasing or is <1000 ml, negative inspiratory force is <20cmH2O, paO2 <70 or the patient is having significant difficulty clearing secretions or is aspirating.

Answer 96

Albuminocytologic dissociation or elevation in cerebrospinal fluid protein (especially IgG) without pleocytosis (lack of nucleated cells). Normal values may be seen on presentation Elevation may not occur until the second week of illness Protein elevation may be very high (greater than 1000 mg/dl) but may not be elevated until symptoms have been present greater than 1 week

Answer 97

early leukocytosis may be seen with a left shift that resolve during the course of the illness.

Answer 98

There is no known cure for GBS, but there are therapies that lessen the severity and accelerate recovery in many patients. Refer to neurology-treatment determined by specialist. Severe acute polyneuropathy is a medical emergency. Initiate therapy as soon as possible following diagnosis. Delayed therapy, even 2 weeks after first motor symptoms, may prove to be ineffective. Admit to ICU for constant monitoring and vigorous support of vital functions. Measure vital capacity and arterial blood gases Intubation may be indicated for the following; vital capacity less than 12-15 ml/kg, partial pressure of oxygen in arterial blood less than 70, negative inspiratory force weaker than 20 cm H20 or rapidly worsening, difficulty clearing secretions, and/or concerns of aspiration. Anticipate respiratory support by mechanical ventilation. Monitor patients with autonomic dysfunction (brady or tachy arrhythmias, orthostatic hypotension, systemic hypertension and hypotension) PRN, as dysautonomia is a leading cause of mortality in patients with GBS Encourage fluid intake to maintain adequate urine output Monitor serum electrolytes Maintain skin integrity, protect skin from trauma and pressure by repositioning frequently. Apply moist heat to relieve pain and permit early physical therapy. Range of motion exercises Nutrition management Assess pharyngeal function Initiate enteric or parental nutrition if patient has trouble swallowing. Emotional support and social counseling

Answer 99

Immunomodulating treatment with intravenous immunoglobulin (IVIG) and plasmapheresis are both considered first line therapy and deemed equivalent in efficacy. IVIG- 0.4 g/kg/day for 5 days (always check serum igA levels before infusion to prevent anaphylaxis in igA-deficient patients) Plasmapheresis: 200 to 250 ml/kg over five sessions every other day, started within 7 days of onset of symptoms Combination of therapies does not offer additional benefit. Corticosteroids are not indicated for patients with GBS. Prevention of thromboembolic events Thromboembolic events are leading cause of mortality in GBS. Heparin (5000 units SQ every 8 hrs) along with sequential compression devices is indicated. Pain management May be significant especially during reinnervation phase. NSAIDS to opiods are suitable Neuropathic pain meds may be beneficial (gabapentin) Stress ulcer prevention, especially those that are on the vent Ranitidine, famotidine, cimetidine

Answer 100

Triad: ophthalmoplegia, ataxia, and areflexia. Demyelinating neuropathy occurs in most patients, but approximately 5% of cases present with primary axonopathy. This subtype, called the Miller Fisher variant, may present with descending paralysis and often involves eye muscles on presentation.

Answer 101

a localized herpes zoster infection involving the seventh nerve and geniculate ganglia, resulting in hearing loss, vertigo, and facial nerve palsy.

Answer 102

Triad: Unilateral Facial Palsy, Ipsilateral Otalgia, erythematous vesicular rash on either the auricle or oral mucosa. Other symptoms include: altered taste perception, saliva/tear production, Hearing loss, Vertigo. First presentation typically pain, then the development of the Varicella Zoster Rash, then facial weakness develops reaching a maximum by approximately 1 week after onset. The facial weakness is unilateral and affects all muscles of facial expression.

Answer 103

Distinguish betweenlower motor neuron (peripheral) and upper motor neuron (central) facial muscle weakness. This can be done by asking the pt to “close your eyes” (which tests upper facial area) and “show me your teeth” (which tests lower facial area). Pt with lower motor neuron weakness will have weakness or paralysis of all muscles of facial expression

Answer 104

Antiviral Therapy is the first 72 hours of presentation is the standard treatment. Acyclovir 500mg x5/day x 1week or Valcyclovir 1000mg TID x 1week, but if pt is renal insufficient, drug dosage is based on pt’s creatinine clearance. Corticosteroids are usually given in the absence of contraindications, but be aware of the side effects of corticosteroids like osteoporosis, increased blood glucose, possible development of DM. Pts with significant pain, particularly over 60yo, use of gabapentin or pregabalin to decrease the post-herpetic neuralgia should be considered. Pts with decreased tear production and inability to close the eye on affected side are at risk for corneal abrasion and should be encouraged to use saline wetting drops frequently.

Answer 105

Ophthalmology referral if corneal damage/ulceration occurs. ENT referral if significant nerve impairment or development of synkinesis.

Answer 106

Sudden onset of lower motor neuron Facial Palsy Hyperacusis or impaired taste may occur No other neuro abnormalities Face often feels stiff and pulled to one side. There may be ipsilateral restriction of eye closure and difficulty with eating and fine facial movements. A disturbance in taste is common(chorda tympani fiber involvement) and hyperacusis due to involvement of fibers to the stapedius . If related to herpes zoster infection, vesicles may be seen in external ear canal.

Answer 107

60% of cases resolve without treatment. Treatment with corticosteroids (prednisone 60mg orally daily for 5 days, followed by 5-day taper, or prednisolone 25mg BID for 10days) Tx with acyclovir or valacyclovir only indicated when there are herpatic vesicles in external ear canal It is helpful to protect the eye with lubricating drops and a patch if eye closure is not possible.

Answer 108

Trigeminal neuralgia is an intense, usually unilateral paroxysmal, stabbing pain in the sensory distribution of the trigeminal (cranial nerve V) nerve.

Answer 109

-Idiopathic, likely an aberrant artery or vein compressing cranial nerve V at or near the pons. Symptomatic: Saccular aneurysm, Arteriovenous malformation, Tumors/mass-lesions at cerebellopontine angle, (Vestibular schwannoma, Meningioma, Epidermoid) - Primary demyelinating disorders: - MS - Charcot-Marie-Tooth disease - Infiltrative disorders: trigeminal amyloidoma -Nondemyelinating lesions: Small infarct or angioma in the brainstem - Familial

Answer 110

Paroxysmal, unilateral facial pain, usually described as shock-like, stabbing or electric Pain can be described as lightning flushes Facial flushing Salivation Headache Pain can be spontaneous or triggered by touch, an air current, or activities such as shaving, eating or brushing teeth In severe cases, facial spasms accompany the pain Pain is usually described in distribution of the second (V2-maxillary) and third (V3-mandibular) divisions of the trigeminal nerve. The pain seldom last few seconds to a minute There is usually sensory or motor loss

Answer 111

Touch, an air current, or activities such as shaving, eating or brushing teeth

Answer 112

Neuroimaging (MRI) should be considered in young patients <40 with atypical symptoms (sensory loss, bilateral symptoms). MRI is useful to identify potential compressors or demyelinating patients. In young patients with trigeminal neuralgia, secondary causes such as MS should be considered and MRI of head obtained.

Answer 113

CT to r/o neoplasm ESR to r/o temporal arteritis

Answer 114

Carbamazepine 400-800mg, 2-3 times daily in divided doses for initial tx. Titrated to pain relief by 100-200 mg every 3 days to max of 1200mg divided BID or TID. Monitor liver enzymes. Oxacarbazepine can be used if carbamazepine is not tolerated due to side effects. Other medications include baclofen, phenytoin, gabapentin, clonazepam, lamotrigine, and levetiracetam

Answer 115

Patients with refractory pain eventually will need secondary intervention such as microvascular decompression, selective nerve fiber destruction, glycerol injection, thermal lesioning, chemical ablation or gamma knife radiosurgery. Microvascular decompression is the only available nodestructive procedure and is effective in 75% of patients. Surgery not appropriate in MS Refer to neurologist

Answer 116

Amyotrophic Lateral Sclerosis is a progressive, degenerative neuromuscular condition of undetermined etiology affecting corticospinal tracts and anterior horn cells, resulting in dysfunction of both upper motor neurons (UMN) and lower motor neurons (LMN).

Answer 117

LMN signs (weakness, hypotonia, wasting, fasciculations, hyporeflexia or areflexia) • UMN signs (loss of fine motor dexterity, spasticity, extensor plantar responses, hypereflexia, clonus) • Preservation of extraocular movements, sensation, bowel and bladder function • Dysarthria, dysphagia, pseudobulbar affect, frontal lobe dysfunction • Respiratory insufficiency typically occurs late in the disease

Answer 118

Riluzole (Rilutek), a glutamate antagonist, is the only FDA-approved medication known to extend tracheostomy-free survival in patients with ALS. Dose is 50mg q12h, at least 1 hr before or 2 hr after meals. May prolong survival by 2-3 months. Check ALT 1x mo for 3 mo initially, followed by once q 3 mo until 1 yr therapy completed, then check periodically. * Sialorrhea (Hypersalivation), may respond to either glycopyrrolate or amitriptyline (consider either propranolol or metoprolol if secretions are thick). Botulinum toxin may be effective in medically refractive cases. * Spasticity may be treated with baclofen, tizanidine, clonazepam * Pseudobulbar affect (Inappropriate involuntary laughing and crying) may improve with amitriptyline, sertraline, or dextromethorphan/quinine.

Answer 119

Electromyography may show changes of chronic partial denervation, with abnormal spontaneous activity in the resting muscle and a reduction in the number of motor units under voluntary control. In patients with suspected SMA (spinal muscular atrophy) or ALS, the diagnosis should not be made with confidence unless such changes are found in at least 3 spinal regions (cervical, thoracic, lumbosacral) or 2 spinal regions and the bulbar musculature. Motor conduction velocity is usually normal but may be slightly reduced, and sensory conduction studies are also normal.

Answer 120

Mean duration of symptoms is 3 – 5 years. Approx 20% of patients survive >5yr.

Answer 121

Noninvasive positive-pressure ventilation may improve quality of life and may increase tracheostomy-free survival in patients with respiratory difficulty (defined by orthopnea or FVC 50% predicted). * PEG tube placement improves nutritional intake, promotes weight stabilization, and eases medication administration. Some studies suggest PEG may prolong life 1-4 mo * Nutrition, speech, physical, and occupational therapy * Suction device for sialorrhea * Cough assist device for ineffective coughing & to maintain a clear airway * Communication may be eased with computerized assistive devices * Early discussion of living will, resuscitation orders, desire for PEG, trach, potential LTC * Encourage contact with local support groups

Answer 122

Progressive neurodegenerative disorder caused by degeneration of Dopaminergic neurons in the substantia nigra pars compacta.

Answer 123

Resting tremor –Often asymmetric, Disappears with voluntary movement, Often initially emerges in one hand while walking – may present as “pill rolling”, May also present in jaw, chin, lips, and tongue Rigidity – “Cogwheel” = catching and releasing, Lead pipe” = continuously rigid Bradykinesia – moving slowly Postural instability Decreased emotion displayed in facial features General motor slowing and stiffness – one or both arms do not swing with walk Speech soft; mumbling Falls; difficulty with balance – tends to occur with disease progression

Answer 124

Dopamine depletion in the substantia nigra and the nigrostriatal pathways -- this results in major motor complications. Pathologic Hallmark = selective loss of Dopamine-containing neurons in the pars compacta of the substantia nigra Loss of neurons accompanied by presence of Lewy Bodies, pale bodies (predecessor of the Lewy Body), and Lewy neuritis Genetic factors have been linked to Parkinson’s -- especially if onset is <50 yo Risk:Age and family Hx of PD or tremor are the greatest risk factors

Answer 125

GOAL = To improve motor and nonmotor deficits o No tx is shown to slow progression Rehab with PT and OT – to improve functional outcomes Physiotherapy to help with gait re-education; improve movement limitations; improve functional independence Home safety Emotional/psych support Speech therapy Treat Non-motor symptoms ED – Sildenafil Constipation – Polyethylene Glycol Surgery Deep brain stimulation – if pt does not have dementia or depression and is otherwise healthy

Answer 126

First Line (in early Parkinson’s) = Carbidopa + Levodopa (Sinemet.); Helps with Bradykinesia and periodic limb movements, Most pts will eventually experience motor fluctuations with Levodopa use, ALL pts will eventually require Levodopa Dopamine Agonists (Pramipexole); SE = nausea, vomiting, hypotension, sedation, edema, vivid dreaming, compulsive behavior, confusion, lightheadedness, hallucinations MAO-B Inhibitors (Rasagiline): Can be considered for initial monotherapy, SE = insomnia, jitteriness, hallucinations Second Line = Beta-adrenergic antagonists (postural tremor), Amantadine, Anticholinergics (only useful in young pts with tremor)

Answer 127

a medical neurologic emergency that carries a HIGH risk of mortality. Historically defined as 30 minutes of continuous seizure activity or 2 or more seizures without full recovery of consciousness between seizures. In practice, a continuous seizure that lasts >5 minutes is treated as status epilepticus - Aggressive treatment is required for a patient with continuing seizures lasting 5-10 minutes or seizures without intervening consciousness - Status epilepticus is a medical emergency requiring immediate treatment - The longer the seizure activity lasts, the more difficult to control seizure

Answer 128

BENZODIAZAPINES (1st line treatment as they are able to rapidly control seizures): Lorazepam (Ativan) OR Diazepam (Valium) OR midazolam (Versed). If no IV access: Midazolam IM ANTI-CONVULSANTS: Phenytoin (Dilantin) administered WITH Lorazepam or Diazepam and NS for long term control (CANNOT give Phenytoin with glucose-containing products as it will precipitate), Fosphenytoin (Cerebyx) – may be administered INSTEAD of Phenytoin (DOES NOT irritate veins, can be given with all common IVF, and can be given quicker than Phenytoin, but is more expensive) MUST MONITOR for arrhythmias with either anti-convulsant** **DO NOT abruptly withdraw anticonvulsant from a patient; taper drugs If seizures CONTINUE: Intubate Administer Phenobarbital (Luminal): Respiratory depression and hypotension are common with Phenobarbital May alternate/additionally add Valproic Acid (Valproate), although not FDA approved for status If still unsuccessful after 60 minutes Consider Propofol (Diprivan) After getting control of status epilepticus, an oral drug program for long-term management is started, and investigating the cause of the disorder

Answer 129

Initial management is SUPPORTIVE Maintenance of airway and 50% dextrose (25-50mL) IVF in case hypoglycemia is responsible

Answer 130

- ABRUPT discontinuation/poor adherence of anti-epileptic drugs - Acute neurologic injury (ischemic or hemorrhagic stroke, meningitis) - CNS infections - Traumatic Head injury - CNS toxicity : certain medications, drugs, ethanol - Brain tumors or other mass lesions - Metabolic disturbances: HYPOGLYCEMIA, hyponatremia - Cryptogenic

Answer 131

cortical discharges localized within one cerebral hemisphere. Focal seizures can involve impairment of consciousness and may evolve to convulsive seizures.

Answer 132

A. Consciousness is preserved and rarely last longer than 1 minute. b. Jacksonian March movements- Manifested by focal motor symptoms (convulsive jerking), or somatosensory symptoms (paresthesia or tingling) that spreads to different parts of the limb or body.. c. Todd’s paralysis: localized paresis in the involved region lasting mins to hrs d. sensory symptoms- light flashing or buzzing, illusions or structured hallucination, alterations in taste, olfactory changes; e. autonomic symptoms- abnormal epigastric sensations, sweating, flushing, pupillary dilation; f. dysphasia; nausea; deja vu; fear; distortion of time perception

Answer 133

a. MOST COMMON SEIZURE in EPILEPTICS- any simple partial seizure onset followed by impairment of consciousness. b. Automatisms may occur : lip smacking, chewing, swallowing, sucking, picking at clothes c. May begin with a stare at the time of consciousness in impaired d. usually begins with an aura

Answer 134

Sudden loss of consciousness (5-30 sec) with eyes fluttering or muscle spasms begins and ends quickly and may not be apparent; common in children 6-14yrs; enuresis; and may have mild clonic, tonic, or atonic components; can accompany automatisms

Answer 135

Alteration in consciousness typically last longer; accompanied by motor signs; less responsive to anticonvulsants; may be accompanied with developmental delay or mental retardation

Answer 136

consist of single or multiple myoclonic jerks

Answer 137

often begins abruptly with an outcry characterized by a sudden loss of consciousness, rigidity(tonic phase) and fall to the ground and respiration is arrested; then contractions of the muscles of the extremities truck and head(clonic phase); commonly urinary incontinence; Last approx 2-5 min; followed by a postictal state (ie. deep sleep, headache, muscle soreness, amnesia of events, nausea, confusion)

Answer 138

a series of seizures lasting longer than 5 min with the patient never returning to baseline between seizures

Answer 139

consist of brief (less than 2 seconds) loss of muscle tone and results in fall known as Epileptic drop attack.

Answer 140

1. TIA’s- longer duration, lack of spread, and negative symptoms (weakness, or numbness). 2. Migraine aura- may produce negative or positive (convulsive jerking or paresthesia) symptoms; tends to spread slowly from one part of the body to another (over mins instead of seconds) and is usually longer in duration (min to hrs). 3. Panic attacks-hard to distinguish from focal seizures unless evidence of anxiety disorder between attacks and the attacks have a clear relationship to external circumstances. 4. Rage attacks- situational and lead to goal directed aggressive behavior.

Answer 141

1. Syncope-rapid recovery with recumbency- NO postictal headache or confusion. However in some instances motor accompaniments and urinary incontinence may simulate a seizure. 2. Cardiac dz- cerebral hypoperfusion due to cardiac rhythm disturbance should be suspected in patients with episodic LOC. 3. Brainstem ischemia- LOC is preceded by other brainstem signs. 4. Psychogenic nonepileptic seizures (PNES)- Conversion disorder or malingering that simulate epileptic seizure; hx of childhood physical/sexual abuse is common; Usually occurs during times of stress; eyes usually forcibly closed; rarely leads to injury; goal directed behavior or shouting; no elevation in prolactin levels

Answer 142

Acidosis, Electrolyte imbalances (hyponatremia, hypocalcemia), Hypoglycemia, Hypoxia, **Alcohol or barbiturate withdrawal are themost common causes of new onset seizures in adults

Answer 143

Pediatric age groups- d/t congenital abnormalities Unknown Etiology Metabolic disorders (see above) CNS infection Head trauma Tumors and other space occupying lesions Vascular dz (common with advanced aging and the most common cause of onset of seizure disorder at 60yrs of age) -Degenerative disorders -Alzheimer’s dz ****The MOST common cause of seizures is non compliance with a drug regimen in a pt with diagnosed epilepsy

Answer 144

-Obtain a history from patient and family or observers of the even -24hr continuous EEG to support dx of epilepsy, differentiate between types of seizures, and to provide a guide to prognosis -CT head/MRI for all new onset seizures (r/o neoplasm) -LP- assess for infectious process after ct/mri -Blood- CBC, Glucose, liver/renal function, VDRL, electrolytes, Mg, Ca, Antinuclear antibody, ESR, ABG, Urine drug test, Serum prolactin (rises 2-3 times normal for 10-60 min after the occurrence of 80% tonic-clonic or complex seizures)

Answer 145

Phenytoin (Dilantin)- 10-20 mcg/ml

Answer 146

PHenobarbital- 15-30 mcg/ml for epilepsy control

Answer 147

sudden or rapid onset of neurologic deficit caused by focal ischemia that lasts for a few minutes and resolves completely within 24 hours. Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction on MRI. Symptoms typically resolve within 60 minutes and almost always within 24 hours.

Answer 148

embolic (10-15%), large vessel atherothrombotic disease (20-25%), lacunar disease, hypoperfusion, hypercoagulable state, arteritis. Atrial septal defects and patent foramen ovale may permit venous thromboemboli to reach the brain (paradoxical emboli). Vasculitis conditions such as moyamoya disease, fibromuscular dysplasia, lupus, and others Hematologic causes: Platelet disorders, oral contraceptive and/or estrogen use, antithrombin III deficincy, hypercoagulable conditions, Myeloproliferative disorders, leukemia with WBW greater than 150,000. Intracranial causes: brain tumor, focal seizure, hemorrhage (SDH, SAH, ICH {which may cause carebrovascular dysfunction due to leakage of blood outside the normal vessels). Subclavian steal syndrome: localized stenosis or occlusion of a subclavian artery proximal to the source of the vertebral artery, so that blood is stolen from that artery; BP is significantly lower in the affected arm than in the opposite arm, bruit in the supraclavicular fossa, and unequal radial pulses. Others: transient hyptotension, osteophytes that cause compression of the neck vessels, cocaine abuse, hypoglycemia, migraines.

Answer 149

5-10% of pts with TIA will have a stroke within 90 days. The risk of stroke is high in the first 3 months after an attack, particularly in the first month and especially within the first 48 hrs.

Answer 150

Rapid onset of a neurologic deficit involving ischemia to certain vascular territory and lasting longer than 24 hrs A stroke in evolution is an enlarging infarction manifested by neurologic defects that increase over 24-48hrs

Answer 151

80% of strokes are caused by blood clots that produce ischemic areas in the brain; remaining 20% of strokes are caused by ICH. Cocaine-related stroke is increasingly common. Women who use oral contraceptives and who smoke are at high risk HLD raises the risk of ischemic stroke Low cholesterol increases the risk of hemorrhagic stroke.

Answer 152

small lesions that occur in the distribution of short penetrating arterioles in the basal ganglia, pons, cerebellum, internal capsule, thalamus, and deep cerebral white matter; usually associated with poorly controlled HTN or DM; contralateral pure motor hemiparesis or pure hemisensory deficit, ipsilateral ataxia with hemiparesis, and dysarthria with clumsiness; may progress over 24-36 hrs before stabilizing. Prognosis good.

Answer 153

thrombotic or embolic occlusion of a major vessel; leads to release of excitatory and other neuropeptides that may augment calcium flux into neurons, thereby leading to cell death and increasing the neurologic deficit.

Answer 154

Sudden onset of a focal neurologic deficit as a result of a cerebral ischemia resulting in cell death.

Answer 155

atherosclerosis, cardioembolism, artery to artery embolism, small-vessel lipohyalinosis, arterisis, arterial dissection and vasospasms. Caused by a thrombus that occludes a blood vessel in the head or neck (30%): Progression of symptoms over hours to days or can be sudden, pts often have a hx of TIA, Predisposing factors: atherosclerosis, HTN, DM, hyperlipidemia, vasculitis, hypotension, smoking, connective tissue disorders, trauma to the head and neck. Caused by embolism (25%): Very rapid onset, hx of TIA. predisposing factors: A-fib, mitral stenosis and regurgitation, endocarditis, and mitral valve prolapse.

Answer 156

Sudden onset of a focal neurologic deficit caused by hemorrhage into or around the brain Condition resulting from bleeding into the subarachnoid space or brain parenchyma Accounts for approx 14% of all cerebral infarction

Answer 157

HTN, use of anticoagulants or thrombolytics, use of illicit street drugs (cocaine), heavy use of alcohol, hematologic disorders.

Answer 158

hemiplegia {involves upper extremities and face more often than lower extremity), hemianesthesia, hemianopia {blindness of half the field of vision}, eyes may deviate to the side of the lesion, aphasia if dominant hemisphere is involved, neglect syndrome, occlusion of various branches of the middle cerebral artery may cause different findings (involvement of the anterior division may cause expressive aphasia, and involvement of the posterior branch may produce receptive aphasia).

Answer 159

unilateral hemianopia; blindness with anosognosia (anton syndrome) if bilateral.

Answer 160

lateral medullary (Wallenburg’s) syndrome ipsilesional loss of pinprick and temperature on the face and contralateral loss of pinprick and temperature on the body; ipsilesional Horner’s syndrome and ipsilesional palatal weakness with resulting dysphagia, dysarthria, vertigo, nystagmus, ataxia.

Answer 161

hemiplegia {lower extremity more often than upper extremity), primitive reflexes, confusion, abulia, bilateral anterior infarction may cause behavioral changes and disturbance in memory.

Answer 162

decreased LOC, vertigo, N/V, diplopia, quadriparesis or quadriplegia, locked in syndrome, dysphagia, ipsilateral cranial nerve findings, contralateral (or bilateral) sensory and motor deficits.

Answer 163

most common, less than 5mm in diameter, associated with poorly controlled HTN and DM, contralateral pure motor or sensory deficits, ipsilateral ataxia with crural (pertaining to the leg or thigh) paresis, dysarthria with clumsiness of the hand.

Answer 164

Sudden HA of intense severity that radiates into the posterior neck region and is worsened by neck and head movements; often described as a thunderclap HA, or worst headache of my life.

Answer 165

Grade I: asymptomatic or slight HA Grade II: moderate to severe headache, stiff neck, no focal signs other than cranial nerve palsy. Grade III: drowsy, mild focal deficit, or confusion Grade IV: stupor hemiparesis Grade V: deep coma, decerebration

Answer 166

Grade I: no blood detected Grade II: diffuse or vertical layers less than 1 mm thick Grade III: localized clot and/or vertical layer 1mm or more Grade IV: intracerebral or intraventricular clot with diffuse or no SAH.

Answer 167

Elevation of BP often to very high levels (90%) of patients. HA (40%) Vomiting is an important diagnostic sign particularly if the hemorrhage lies in the cerebral hemisphere (49%). Sudden onset of neurologic deficits that can repidly progress to coma or death, depending on area involved (50%), Basal ganglia hemorrhage (conjugate deviation of eyes to the side of the lesion, decreased LOC, contralateral hemiplegia, hemisensory disturbance) Thalamic hemorrhage (downward deviation of eyes, looking at the nose, pupils pinpoint with a positive reaction, coma is common, flaccid quadriplegia. Cerebellar hemorrhage (ipsilateral lateral conjugate gaze paresis, PERRL, inability to stand or walk, facial weakness, ataxia of gait, limbs or trunk, vertigo and dysarthria. Pons and lobar (amyloid angiopathy)

Answer 168

ICH score: GCS (0-2 points), pt age >80 (1 point), ICH volume >30ml (1 point), presence of intraventricular blood (1 point), and infratentorial origin of blood (1 point). Scores range from 0 to 6 with a score of 0 conferring )% mortality and a score of 6 with estimated 100% mortality.

Answer 169

distal to its junction with the anterior communicating artery causes weakness and cortical sensory loss in the contralateral let and sometimes mild weakness of the arm, especially proximally. Contralateral grasp reflex, paratonic rigidity, abulia (lack of initiative), or frank confusion. Urinary incontinence is not uncommon. Bilateral - Marked behavioral changes and memory disturbances. Unilateral - well tolerated because of the collateral supply from the other side.

Answer 170

contralateral hemiplegia, hemisensory loss, and homonymous hemianopoia (bilaterally symmetric loss of vision in half of the visual fields), with the eyes deviated to the side of the lesion. Dominant hemisphere is involved, global aphasia is also present. Considerable swelling of the hemisphere during the first 72 hours. Impossible to distinguish from occlusion of the internal carotid artery. Superior division in the dominant hemisphere may lead to predominately expressive (Broca) asphasia and to contralateral paralysis and loss of sensation in the arm, face, and to a lesser extent the leg. Inferior branch of dominant produces a receptive (wernicke) aphasia and a homonymous visual field defect. With involvement of the nondominant, speech and comprehension are preserved but there may be left hemispatial neglect syndrome or constructional and visuospatial deficits.

Answer 171

leads to sudden painless visual loss with retinal pallor and a macular cherry red spot on fundoscopic examination. Sudden, transient vision loss in one eye (amaurosis fugax) is a TIA in this arterial territory. Patients with a cilioretinal artery (25%), may have macular sparing due to collateral blood supply.

Answer 172

lead to a thalamic syndrome in which contralateral hemisensory disturbance occurs, followed by the development of spontaneous pain and hyperpathia Often a macular sparing homonymous hemianopia and sometimes a mild, usually temporary hemiparesis. Depending on the site of the lesion and the collateral circulation the severity of these deficits varies and other deficits may also occur including involuntary movements and alexia. Occlusion of the main arery beyond the origin of its penetrating branches may lead solely to a macular sparing hemianopia.

Answer 173

below the origin of the anterior spinal and posterior inferior cerebellar arteries may be other vertebral artery May be clinically silent b/c the circulation is maintained by the other vertebral artery. If remaining vertebral artery is congenitally small or severly athrosclerotic, a deficit similar to that of basilar artery occlusion is seen unless there is good collateral circulation from the anterior circulation through the circle of Willis.

Answer 174

or obstruction of the vertebral artery just before it branches to the vessel leads to the lateral medullary syndrome characterized by vertigo and nystagmus (vestibular nucleus), ipsilateral spinothalamic sensory loss involving the face (trigeminal nucleus and tract), dysphagia (nucleus ambiguus), limb ataxia (inferior cerebellar peduncle) and Horner syndrome (descending sympathetic fibers, combined with contralateral spinothalamic sensory loss involving the limbs.

Answer 175

leads to coma with pinpoint pupils, flaccid quadriplegia and sensory loss, and variable cranial nerve abnormalities. Partial basilar - diplopia, visual loss, vertigo, dysarthria, ataxia, weakness, or sensory disturbances in some or all limbs, and discrete cranial nerve palsies. Hemiplegia of pontine origin - the eyes are often deviated to the paralyzed side, whereas in patients with a hemispheric lesion, the eyes commonly deviate from the hemiplegic side. Small paramedian arteries arising from the basilar artery are occluded, contralateral hemiplegia and sensory deficit occur in association with ipsilateral cranial nerve palsy at the level of the lesion.

Answer 176

S/S: vertigo, N/V/, nystagmus, and ipsilateral limb ataxia. Contralateral spinothalamic sensory loss in the limbs Deafness due to cochlear infarction may follow occlusion of the anterior inferior cerebullar artery, which may also cause ipsilateral facial spinothalamic sensory loss and weakness. Massive cerebellar infarction may lead to obstructive hydrocephalus, coma, tonsillar herniation and death.

Answer 177

No cortical signs are present in lacunar syndromes Pure motor hemiparesis; typically due to an ischemic lesion in either the internal capsule or pons. Pure sensory stroke: typically due to an ischemic lesion of the thalamus,. Ataxic hemiparesis: ataxia out of proportion to the hemiparesis; typically due to an ischemic lesion of either the internal capsule or pons. Sensorimotor stroke: typically due to ischemic lesion involving both the thalamus and internal capsule. Dysarthria-clumsy hand syndrome: multiple localizations possible but typically the pons; facial weakness, dysarthria, and mild clumsiness and weakness of the hand.

Answer 178

Small (<5mm) lesion in the basal ganglia, pons, cerebellum or internal capsule. MRI with diffusion -weighted sequences usually defines the area of infarction; CT is insensitive acutely but can be used to exclude hemorrhage. Lacunar infarcts appear as small, punched-out, hypodense areas Initial CT scan may be negative, and the infarct may not be visible for up to 24hrs

Answer 179

Airway and breathing should be maintained • Supplemental Oxygen should be provided to keep the oxygen saturation >92% • Pneumatic compression devices or pharmacological means should be applied to help prevent deep venous thrombosis • Avoid any and all oral intake until swallowing is clearly unimpaired; this helps to prevent aspiration pneumonia • Early mobilization for rehab is desirable • Consider neurosurgical intervention for craniectomy in select cases. Typical cases in which craniectomy may be performed include cerebellar ischemia with compression of the brain stem and/or the fourth ventricle as well as large middle cerebral artery ischemia. Available evidence suggest that it may be better to preform early hemicraniectomy (,48hr) to achieve better outcomes. Decompressive hemicraniectomy has shown good benefit in terms of mortality but not much benefit in terms of disability and functional outcomes.

Answer 180

IV T-PA, or alteplase, is the only medical therapy approved by the U.S FDA for the treatment of acute ischemic stroke. • The time window for administration is generally accepted to be within 4.5 hours of symptom onset, although the FDA indication is still within 3 hours. The American heart association/ America stroke association recommends a t-PA administration window of up to 4.5 hours with certain additional criteria when compared to the 3 hour administration • • The protocol is weight based with 90mg being the maximum allowable dose. • The risk of brain hemorrhage with IV t-PA is about 6% in stroke patients

Answer 181

• Clinical presentation consistent with an ischemic stroke with clearly demonstrable neurologic deficits • Noncontrast CT head without evidence of hemorrhage • Time since onset of symptoms (or last known normal if time of onset not known) clearly <3 hr (3-4.5 hr with additional exclusion criteria) before TPA administration would begin • Age ≥18 years Criteria for excluding TPA as a treatment option: • Absolute exclusion criteria: • Historic and clinical findings suggestive of subarachnoid hemorrhage, even if CT scan is normal 1. Sudden, severe headache, often with a loss of consciousness at onset 2. Vomiting • Active internal bleeding, increased risk of bleeding, or known bleeding diathesis, including those resulting from: 1. Recent use of warfarin with an INR of ≥1.7 2. Use of heparin within 48 hr with a prolonged aPTT 3. Current use of direct thrombin inhibitors or factor Xa inhibitors 4. Platelet count of <100,000/mm3 5. History of intracranial hemorrhage 6. Known intracranial neoplasm, arteriovenous malformation or aneurysm 7. Arterial puncture at a noncompressible site within the past 7 days • Stroke, intracranial surgery, or head trauma within the previous 3 mo • Systolic blood pressure >185 mm Hg or diastolic blood pressure >110 mm Hg that does not decrease below that range with treatment • Blood glucose <50 mg/dl or >400 mg/dl • CT findings: 1. Evidence of intracranial hemorrhage 2. Hypodensity or effacement of the sulci in one third of the territory of the middle cerebral artery

Answer 182

• Major surgery or serious trauma within the preceding 14 days • Acute myocardial infarction (recent within the previous 3 months) or postmyocardial infarction pericarditis • GI or GU bleeding within the past 21 days • Seizure at stroke onset • Rapidly improving neurologic signs or Isolated mild neurologic deficits • Patient who is pregnant or lactating Additional exclusion criteria for administering IV tPA in the 3-4.5 hour window • Age >80 years • High stroke scale on presentation (NIHSS >25) • Current use of oral anticoagulants regardless of INR Prior history of stroke and diabetes mellitus

Answer 183

Elevated blood pressure is common during acute stroke and it often subsides without specific therapy. In general hypertension is not treated acutely unless it is extremely hard (example greater than 220 systolic blood pressure) there is evidence of hypertension induced organ damage or thrombolysis is being considered in which case the blood pressure needs to come down ( if it can be safely accomplished) to less than 185/110. It is risky to decrease blood pressure dramatically and quickly in the presence of acute ischemic stroke as it can cause an extension of the infarct tissue into the ischemic penumbra. A 15% to 25% decrease over the first 24 hours is recommended

Answer 184

The presence of systemic hypotension in acute ischemic stroke portends a poor outcome. The cause should be sought and volume depletion should be corrected with normal saline. Cardiac arrhythmias should be treated. Induced hypertension with vasopressor agents may be useful for select cases with an ischemic penumbra that is at risk, but caution is strongly advised

Answer 185

Urgent neurosurgical evaluation is needed in many cases either for evacuation of the hematoma or for relieving raised intracranial pressure by procedures such as EVD placement or decompressive surgeries. • Surgery should be performed promptly for cases of cerebellar hemorrhage of >3 cm when the patient is deteriorating clinically, showing brainstem edema or hydrocephalus. • Surgery for lobar or deep brain clots may be considered for select cases, Although the level of evidence for efficacy is not high. Currently, guidelines recommend standard craniotomy for patients with lobar clots >30 ml within 1 cm. • Recent innovative surgical techniques, such as instillation of thrombolytic agents for intraventricular hemorrhage and minimally invasive surgery for hematoma evacuation, appear to be promising. Clinical trials are currently in progress to assess whether these approaches improve mortality and neurologic outcomes.

Answer 186

The cornerstones of medical management of acute intracerebral hemorrhage include: Control of hypertension Correction of coagulopathy Management of elevated intracranial pressure Treatment of seizures

Answer 187

Blood pressure should be quickly lowered by 15% and then gradually and safely brought to the individual patient’s target range. In theory, this may diminish the expansion of the hematoma. More aggressive control of systolic blood pressure (SBP) to 140 or less in the acute setting has been shown to be safe in clinical trials (INTERACT2 trial) with slightly improved outcomes compared to less aggressive BP control (target SBP <180) and is currently recommended by the American Heart Association/American Stroke Association guidelines.

Answer 188

SBP of >200 mm Hg or MAP of >150 mm Hg: Consider the aggressive reduction of BP with continuous intravenous infusion, with BP monitoring every 5 min. SBP of >180 mm Hg or MAP of >130 mm Hg with evidence or suspicion of elevated ICP: Consider ICP monitor and reducing BP with intermittent or continuous intravenous medications to keep cerebral perfusion pressure >60 to 80 mm Hg. 3. SBP of >180 mm Hg or MAP of >130 mm Hg without evidence or suspicion of elevated ICP: Consider a modest reduction of BP (e.g., MAP of 110 mm Hg or target blood pressure of 160/90 mm Hg) with intermittent or continuous intravenous medications, and clinically reexamine the patient every 15 min.

Answer 189

Early hematoma expansion has been associated with poor outcome. • Protamine sulfate is used to treat cases of heparin-induced intracerebral hemorrhage. Protamine dosage is 1 mg IV for every 100 units of heparin administered in the previous 2 to 3 hours (maximum dose is 50 mg). • Prothrombin concentrate complex (PCC) is now recommended for reversal of warfarin associated ICH. FFP may also be used for this purpose, although it carries the disadvantage of administering more volume, potentially leading to complications such as pulmonary edema and slightly longer times to reversal of coagulopathy compared to PCC. Vitamin K should be administered IV along with flash-frozen plasma (FFP)/PCC for sustained effects. Routine use of recombinant factor VII concentrates is not recommended due to insufficient evidence and concern for increased risk of thromboembolic events. • Idarucizumab (Praxbind) is a humanized monoclonal antibody fragment that can be used for urgent reversal of the anticoagulant effect of the direct thrombin inhibitor dabigatran (Pradaxa). • Andexanet alfa, a recombinant modified human factor X2 decoy protein has been effective for reversion of the anticoagulant effect of apixaban (Eliquis), rivaroxaban (Xarelto), and edoxaban (Savaysa). • Recommendations for thrombolytic-associated intracerebral hemorrhage treatment include the consideration of the infusion of platelets and cryoprecipitate. • Hemostatic therapy has not been shown convincingly to improve outcomes, despite reducing hematoma expansion. Efforts are under way to identify patients at high risk of early hematoma expansion by using clinical and radiographic information to determine who may benefit from more aggressive hemostatic intervention.

Answer 190

This condition should be treated with a graded approach, which may include the elevation of the head of the bed, analgesia/sedation, hyperventilation, and osmotic therapy. In patients clinically suspected to have elevated ICP or with GCS <8, invasive monitoring of the ICP may be required. If conservative treatment fails to control ICP, EVD placement or other decompressive procedures like craniotomy should be pursued.

Answer 191

If seizures occur, they should be treated aggressively, including with intravenous medications, if needed. Although widely practiced, routine use of prophylactic antiepileptic medications is not recommended. Continuous EEG monitoring should be employed in patients with suspected seizures or unexplained low levels of consciousness.

Answer 192

Hyperglycemia: a high blood glucose level predicts a worse outcome. Markedly elevated glucose levels should be lowered to <200 mg/dl. • Antipyretics should be administered for fever in addition to searching for a cause of the fever. • Care should be taken to avoid hypoxia. Airway and ventilatory management should happen early and concurrently with the primary management of ICH. • Pneumatic compression devices should be applied to help prevent deep venous thrombosis. Chemical DVT prophylaxis can be started after 48 to 72 hours in most situations once the bleed has been determined to be stable. • Early mobilization for rehabilitation is desirable

Answer 193

CSF can help exclude SAH by the following two criteria: CSF RBC count <2,000 and no xanthochromia If SAH is present CSF will be uniformly grossly bloody, although this may not occur if the bleed is small. Xanthochromia is present. Yellowish discoloration of CSF produced by blood breakdown products. Xanthochromis appears no earlier than 2-4 hours after bleeding.

Answer 194

1. The 90-day risk of stroke after TIA is 17% 2. The greatest risk is within the first week 3. Approximately one third of stroke patient have a history of TIA

Answer 195

A CT scan of the head (without contrast) should be performed immediately, before the administration of aspirin Or other antithrombotic agents, to exclude cerebral hemorrhage CT is relatively insensitive to acute ischemic stroke within the first 6–12 hours, and subsequent. MRI with diffusion-weighted sequences helps define the distribution and extent of infarction as well as exclude tumor or other differential considerations. If patients present within 6 hours of stroke onset, CT angiography of the head and neck should be performed to identify large vessel occlusions amenable to endovascular therapy. Regardless of timing of presentation, imaging of the cervical vasculature, by CT angiography, MR angiography, carotid duplex ultrasonography, or conventional catheter angiography, is indicated as part of a search to identify the source of the stroke.

Answer 196

CBC Blood glucose Fasting lipid panel Serum syphilis and HIV in some cases Anitphospholipid antibodies (lupus anticoagulants) V Leiden mutation factor Abnormalities of protein C, protein S, or anithrombin. Blood cultures to rule out endocarditis

Answer 197

Electrocardiography or continuous cardiac monitoring for at least 24 hours will help exclude a recent myocardial infarction or a cardiac arrhythmia that might be serving as a source of embolization.

Answer 198

Echocardiography (with agitated saline contrast) should be performed in cases of nonlacunar stroke to exclude valvular disease, left to right shunting, and cardiac thrombus.

Answer 199

The most important initial determination is the time at which the patient was last normal; this is considered the time of stroke onset. If patients receive medical attention within 6 hours of stroke onset, a CT and CT angiogram should be performed to rule out hemorrhage and to identify large vessel occlusions. Intravenous thrombolytic therapy with recombinant tissue plasminogen activator (rtPA; 0.9 mg/kg to a maximum of 90 mg, with 10% given as a bolus over 1 minute and the remainder over 1 hour) improves the chance of recovery without significant disability at 90 days from 26% to 39% if given within 3 hours from stroke onset; it is still effective up to 4.5 hours from stroke onset. Treatment should be initiated as soon as possible; outcome is directly related to the time from stroke onset to treatment. Intravenous thrombolysis is approved in Europe for use up to 4.5 hours from stroke onset but only for up to 3 hours in the United States, although off-label use during the 3- to 4.5-hour window is standard.

Answer 200

Only patients with large vessel occlusion (about 20% of patients with acute ischemic stroke) are eligible for embolectomy, which must be performed within 6 hours of stroke onset. Early management of a completed stroke otherwise requires general supportive measures.

Answer 201

Once hemorrhage has been excluded by CT, aspirin (325 mg orally daily) is started immediately unless the patient received thrombolysis, in which case aspirin is initiated after a follow-up CT has ruled out thrombolytic-associated hemorrhage at 24 hours. Anticoagulant drugs are started when indicated, as discussed in the section on TIAs. There is generally no advantage in delay, and the common fear of causing hemorrhage into a previously infarcted area is misplaced, since there is a far greater risk of further embolism to the cerebral circulation if treatment is withheld.

Answer 202

TIA: CT: May reveal “Silent” ischemia or ischemic images, as well as hemorrhage or infarct and SDH Ischemic Stroke: CT scan of head without contrast should be done initially 1. Preferable to MRI in the acute stage to rule out cerebral hemorrhage as MRI is usually not as readily available, especially for patients who present with stroke symptoms and are on anticoagulation therapy, also will rule out abscess, tumor, and SDH 2. Appear as an area of decreased density 3. Lacunar infarcts appear as small, punched out, hypodense areas 4. Initial CT scan may be negative, and the infarct may not be visible for up to 24 hrs CT Early signs of ischemia Hypoattenuating brain tissue Obscuration of the lentiform nucleus Insular Ribbon sign Dense MCA sign Hemorrhagic infarcts

Answer 203

Cerebral edema may exacerbate intracranial hypertension and may require carefully titrated treatment with oral sodium chloride or intravenous hyperosmotic sodium solution. Daily measurement of the serum sodium level allows for the early detection of this complication. Cerebral edema can be reduced with mannitol and / or hypertonic saline solution Mannitol 0.25-1gram/kg IV every 4-6 hours Saline 3% solution, loading dose of 250-300 ml IV over 60 minute, followed by continuous infusion titrated to treatment goal, including 145-155MEq/L and serum osmolality of 310-320mOsm/L Aline 23.4% solution, 30ml IV administered over 30 min or longer, subsequent doses dependent on ICP

Answer 204

Hemiplegia or focal deficit - after delay of 2-14 days post bleed Vasospasm- sometimes leads to significant cerebral ischemia or infarction and increase ICP Acute Hydrocephalus- should be suspected if the patient deteriorates clinically Causes intracranial HTN which requires shunting Repeat CT scan Renal salt-wasting Develops abruptly during the first several days of hospitalization Results in- hyponatremia, cerebral edema, and worsening intracranial HTN Daily Na+ level = early detection Hypopituitarism Occurs as a late complication

Answer 205

Older age Female sex “Nonwhite” ethnicity Hypertension Tobacco smoking High ETOH consumption (>150g per week) Previous symptoms Posterior circulation aneurysms Larger aneurysms

Answer 206

Obtain an LP if CT scan is unavailable or negative and suspicion is high LP is contraindicated in any expanding mass because it may cause herniation A funduscopic examination must be performed prior to the procedure to rule out papilledema if no CT available

Answer 207

CSF fluid will be uniformly grossly bloody, although this may not occur if the bleed is small. In a true SAH, the LP reveals 103-106 RBCs/mm SAH can be differentiated from a traumatic lumbar puncture by the lack of clearing of RBC from the 1st and 4th tube Opening pressure may be elevated Xanthochromia is present Yellowish discoloration of CSF produced by blood breakdown products Xanthochromia appears no earlier than 2-4 hours after bleeding occurs

Answer 208

Sudden intense headache that radiates into the posterior neck region and is worsened by neck and head movements; often described as a “thunderclap headache” or “worst headache of my life” This may be followed by nausea and vomiting and by loss or impairment of consciousness that can either be transient or progress inexorably to deepening coma and death. If consciousness is regained, the patient is often confused and irritable and may show signs of altered mental status. Neuro exam generally reveals nuchal rigidity and other signs of meningeal irritation, except in deeply comatose patients. Some patients experience sx a few hours or days before SAH occurs, these are called “warning leaks”

Answer 209

A CT scan should be performed immediately to confirm hemorrhage (preferable with CT angiography). CT is preferred over MRI because it is faster and more sensitive in detecting hemorrhage in the first 24 hours.

Answer 210

Systolic blood pressure should be lowered to 140 mmHg until the aneurysm is secured (Barkley recommends less than 160 mm Hg) Consider IV titratable nicardipine drip or Labetalol 10 mg IVP Hydralazine, 10-20 mg IVP if patient has bradycardia

Answer 211

Transcranial ultrasound may be used to screen noninvasively for vasospasm, but conventional arteriography is required to document and treat vasospasm (Barkley sts these should be done daily to monitor to vasospasm) Most frequent between days 7 and 10 after aneurysm rupture and resolves after 21 days Calcium channel blockers (Nimodipine) has been shown to reduce the incidence of ischemic deficits from arterial spasm. 60mg Q4H orally for 21 days is given prophylactically to all patients After surgical obliteration, symptomatic vasospasms may also be treated with intravascular volume expansion and induced HTN Transluminal balloon angioplasty is also helpful

Answer 212

Inflammation of the arachnoid, dura mater, and/or the pia mater of the brain or spinal cord (aka the meninges), which is caused by viral, bacterial, or fungal infections.

Answer 213

``` Sinusitis - otitis media - mastoiditis - pneumonia - trauma - congenital malformations ```

Answer 214

NSAIDS Sulfonamides Certain Monoclonal antibodies

Answer 215

an inflammation of the meninges with increased ICP and pleocytosis or increased WBCs in CSF secondary to bacteria in the pia-subarachnoid space and ventricles.

Answer 216

Profound, life-threatening, may be fatal within hours Bacteria attract inflammatory cells and cytokines This causes a breach in the blood brain barrier. Allowing WBCs, fluid, and other infection-fighting particles to enter the meninges Neutrophils gather, making exudates within subarachnoid space. Exudates cause CSF to thicken and flow of CSF is decreased throughout the brain and spinal cord.

Answer 217

(pneumococcal meningitis): most common, most serious bacterial meningitis S/S range from deafness to severe brain damage Occurs most frequently in infants < 2 years, adults with weakened immune systems, and the elderly Rates in children have declined with use of 7-valent conjugate vaccine (Prevnar)

Answer 218

Occurs in schools, colleges, and other group settings Spreads through contact with nasopharyngeal drainage or blood High-risks groups: infants < 1 y/o, those with suppressed immune system, travelers to endemic countries, college students (freshman in particular) who reside in dormitories

Answer 219

At one time the most common; however, H. Influenzae B (Hib) vaccine has greatly reduced number in US Children in daycare are at greatest risk and children without access to vaccines

Answer 220

May occur, in infants, elderly, immunosuppressed

Answer 221

More benign and self-limiting Pia and arachnoid spaces are filled with lymphocytes, but NOT with exudate forms. Higher Frequency in late summer - early fall

Answer 222

less severe: Fever, Headache, Nuchal rigidity, Photophobia, Myalgias, Vomiting, Rash

Answer 223

through cough, saliva, and fecal matter of an infected person

Answer 224

THE MOST COMMON is enterovirus Others: arbovirus, mumps, varicella, herpes simplex 1or 2, measles, rubella, cytomegalovirus, influenza, Epstein-Barr, HIV Fungal causes: MOST COMMON in immunocompromised, particularly AIDS Transmitted through inhalation and bloodstream Most Common form Cryptococcus neoformans (found in bird droppings) Other fungals: Candida albicans (yeast), Coccidioides immitis, Histoplasma capsulatum, aspergillus Also caused by Syphilis

Answer 225

Severe Headache Stiff Neck(nuchal rigidity, meningismus) Photophobia (maybe diplopia) Fever of 101 - 103 degrees F AMS Cranial nerve palsy Seizures Chills, myalgias Nausea/Vomiting Vertigo Exaggerated deep tendon reflexes Coma, Lethargy, Stupor Rash (petechial or purpura fulminans) Dilated, nonreactive pupils Posturing (decorticate/decerebrate) Kernig’s sign Brudzinski’s sign An additional maneuver to assess for meningitis is to elicit jolt accentuation of the patient’s headache by asking the patient to turn his or head horizontally at a frequency of 2-3 times/sec= Worsening of baseline headache is a positive sign

Answer 226

Flext the patient’s head and neck to the chest The legs will flex at the hips and at the knees in response to this movement

Answer 227

Flex the patient’s leg at the knee, then at the hip, to a 90 degree angle, then extend the knee. In the presence of meningitis, this maneuver will trigger pain and spasms of the hamstring muscles caused by the inflammation of the meninges and spinal nerve roots.

Answer 228

Lumbar puncture (LP) should be performed as soon as diagnosis is suspected. But, CT of brain should be completed prior to LP, in patients with: Altered, LOC, papilledema, Neurologic deficits, new-onset seizure, Immunocompromised, hx of CNS disease AFTER collecting H&P and Stat labs including blood cultures x 2.

Answer 229

Performing LPs in the presence of a space-occupying lesion may result in brainstem herniation. IF patient is . . . Comatose Unable to provide hx (no family available) Risk of Mass Lesion Papilledema, focal neurologic deficits, recent head trauma, malignant neoplasm, or Hx of CNS mass lesion Immunosuppressed (HIV, Transplant, neoplasm, steroids) LP is NOT performed - move straight to treatment

Answer 230

Sterile dressing Sterile gloves Sterile drape Antiseptic solution with skin swabs Lidocaine 1% without epinephrine Syringe, 3 mL Needles, 20 and 25 gauge Spinal needles, 20 and 22 gauge Three-way stopcock Manometer Four plastic test tubes, numbered 1-4, with caps Syringe, 10 mL (optional) If in seated position, a bedside table Sterile dressing Sterile gloves Sterile drape Antiseptic solution with skin swabs Lidocaine 1% without epinephrine Syringe, 3 mL Needles, 20 and 25 gauge Spinal needles, 20 and 22 gauge Three-way stopcock Manometer Four plastic test tubes, numbered 1-4, with caps Syringe, 10 mL (optional) If in seated position, a bedside table

Answer 231

Cloudy, elevated opening pressure >180, increased WBCs (100-5000), increased total protein(100-500), decreased glucose (5-40), bacteria present on gram stain

Answer 232

Clear, normal opening pressure(<200), increased WBC (500-1000, most are mononuclear), normal or slightly increased protein (<200), normal glucose(>45), no bacteria on culture

Answer 233

Dexamethasone 10 mg IV q 6 hours x 4 days Ceftriaxone 2 gr IV q 12 hours Vancomycin 1 gr IV q hours Ampicillin 2 gr IV q 4 hours (given for hx of ETOH, organ transplant, malignancy, pregnancy or age great than 50. If treating meningitis in a patient with hx of neurosurgery or head trauma Therapy will be Cefepime and Vancomycin

Answer 234

Rifampin 10 mg/kg po bid x 2 days Rocephin (ceftriaxone) 250 mg IM single dose in patient > 12. Rocephin (ceftriaxone) 125 mg IM single dose in patients

Answer 235

Anticonvulsants: Lorazepam or Diazepam for seizure control Tylenol 325 mg - 1,000 mg q 4 hrs prn pain/fever (not to exceed 3 gr in 24 hours) Fluid replacement with RL or NS, AVOID hypotonic solutions and D5W.

Answer 236

Xanthochromia is the yellowish discoloration of CSF that is indicative of the presence of bilirubin. It is caused by RBC degeneration. Xanthochromia can be detected in as little as 12 hours and can persist up to 2 weeks.

Answer 237

signs of expanding intracranial mass, signs of primary infection or congenital heart dz sometimes present, fever may be absent. May occur as a result as of infection from anywhere in the body but especially in ear or nose

Answer 238

early signs-headache, drowsiness, inattention, confusion and seizures. Late signs- increasing intracranial pressure(nausea, vomiting, altered level of consciousness), focal deficits, and neuro changes (speech and visual disturbances, hemiparesis), and worsening headache. May be little or no evidence of systemic infection.

Answer 239

CT will show area of contrast enhancement surrounding a low density core. Elevated WBCs and sed rate. LP- elevated opening pressure, increase in protein

Answer 240

IV antibiotics (ceftriaxone, metronidazole, and vanco) for at least 6-8 weeks, surgical drainage (aspiration or excision) to decrease mass effect. Dexamethasone/mannitol for edema. Monitor with Serial CTs or MRI scans every 2 weeks. Surgical removal needed if over 2.5 cm. Hyperventilate those on the vent to decrease ICP

Answer 241

give Meningococcal Penicillin G q4h, if allergic, give ceftriaxone or cefotaxime

Answer 242

if beta lactamase negative, give ampicillin; if beta lactamase positive, give ceftriaxone or cefotaxime

Answer 243

Start empiric therapy, give supportive therapy

Answer 244

give INH, pyridoxine, rifampin, pyrazinamide, and ethambutol along with empiric therapy

Answer 245

add dexamethasone to empiric therapy. Give with FIRST antibiotic dose, NOT after regimen has started.

Answer 246

Hemorrhage and edema in TEMPORAL lobes

Answer 247

Infection in the tissues near puncture site--infection may spread to brain. Midline shift Posterior Fossa mass

Answer 248

Increased ICP caused by a space occupying lesion (blood, tumor, or especially brain abscesses)-- LP may cause herniation Coagulopathy Severe thrombocytopenia

Answer 249

Lateralizing signs (hemiparesis) Sign of uncal herniation (unilateral 3rd-nerve palsy with an altered level of consciousness) If pt has clotting deficiency--try to correct before doing the LP; but, ASA and NSAIDs have not been shown to increase risk of bleeding following LP. Pt with prior lumbar fusion or laminectomy

Answer 250

Cardiorespiratory collapse Stupor Seizures Sudden death Herniation--particularly in pts with brain abscesses

Answer 251

1. Obtain consent. 2. Position pt in bed—Lateral decubitus position (side lying) with shoulders and hips perpendicular to bed/table; draw knees to chest; arch pts back out towards provider; may consider mild sedation 3. ID and mark anatomical landmarks—Find anatomic midline at L4 spinous process; it is at the level of the posterior-superior iliac crests. (This is well below the termination of the spinal cord, and the only important neurologic structure is the cauda equina.) Can also use interspaces above/below L4—safe from L2-L3 to L5-S1 interspaces in adults. 4. Prep the skin—apply antiseptic solution in circular motion from the center outward, gradually increasing the circumference 5. Apply sterile drape—with window open to L4 6. Anesthetize—Lidocaine 1% —create a wheal with anesthetic in the skin over the entry site;then anesthetize the deeper tissues. *Ask about anesthetic allergies. 7. Puncture—insert the needle midline in the interspace; use 3.5”, 20ga needle; bevel up towards the ceiling. Hold the needle parallel to the bed; advance slightly upward towards the umbilicus. Remove the stylet occasionally to check for CSF. May feel a “pop” as you pass through the ligamentum flavum and into the subarachnoid space. 8. Visualize CSF—will flow from the needle hub when the subarachnoid space is punctured and the stylet is removed. CSF is normally clear. 9. Attach the manometer—measure the opening pressure; this only works in the decubitus position (not if you do the LP with the pt sitting). May notice fluctuations in the fluid column with respirations and arterial pulsations. 10. Collect CSF—for analysis, collect in sequential numbered vials (usually 4); 1= glucose, protein and electrophoretic studies; 2= microbiologic and cytologic studies; 3= serologic tests; 4=extra 11. Replace stylet before removing needle!!—and observe for signs of cord or spinal nerve compression from a hematoma (may develop within the first several hours in patients with coagulopathy disorder).

Answer 252

Patients with altered LOC Focal neurologic findings > 60 yo Immunocompromised pts Papilledema--seen on PE If brain occupying lesion is suspected or known (especially a brain abscess)--brain abscess greatly increases the risk for herniation Recent seizure--within 1 week of presentation To rule out increased ICP or mass effect--suspected subarachnoid hemorrhage (SAH)

Answer 253

Catheter obstruction--proximal obstruction most common due to tissue debris, blood clots, or choroid plexus within the ventricular catheter: Distal obstruction--due to thrombus or venous occlusion, Peritoneal shunts--associated with infection (peritonitis) or mechanical obstruction (Omental Block) Infection --usually due to skin organisms overlying the valve; may ulcerate the skin and colonize the shunt (Staph Epidermidis, Staph Aureus, gram-neg bacilli); usually occur within the first 2 months after surgery; infection Risk factors = perioperative infection, dental or urologic instrument use Hemorrhage--both intracerebral and subdural. Intracerebral--Usually due to trauma to the brain parenchyma as the catheter is passed through the ventricles; Subdural--due to sudden decompression of the ventricles; leads to tearing of bridging veins as the brain pulls away from the dura--can also be due to overdrainage problems Seizures--infrequent; may give antiepileptic medication if pt is at high risk Shunt fracture Shunt migration Excessive CSF drainage

Answer 254

Long-term management of increased ICP Currently VP shunts are the mainstay for treatment of hydrocephalus--ease of insertion and reliable long-term function

Answer 255

Continued enlargement of ventricles -- they usually diminish in size after shunt placement in pts with high-pressure hydrocephalus (usually within 1 week). Ventricles may remain large despite good shunting in pts with normal-pressure hydrocephalus Signs of increased ICP--such as altered LOC, nausea, vomiting, vision disturbances, fever, diaphoresis, failure of upward gaze (sunset eyes). Should routinely do cranial nerve, visual field and fundoscopic exams

Answer 256

The olfactory nerve (I): smell The optic nerve (II): carries visual information from the retina of the eye to the brain. The oculomotor nerve (III): eye’s movements, pupil size The trochlear nerve (IV): controls rotational movement of eye The trigeminal nerve (V): sensation and motor function in the face and mouth. The abducens nerve (VI): controls lateral movement of eye The facial nerve (VII): controls the muscles of facial expression, taste The vestibulocochlear nerve (VIII): responsible for transmitting sound and equilibrium (balance) information from the inner ear to the brain. The glossopharyngeal nerve (IX): receives sensory information from the tonsils, the pharynx, the middle ear, and the rest of the tongue. The vagus nerve (X): This is responsible for many tasks, including heart rate, gastrointestinal peristalsis, sweating, and muscle movements in the mouth, including speech and keeping the larynx open for breathing. The spinal accessory (XI): controls specific muscles of the shoulder and neck. The hypoglossal nerve (XII): This nerve controls the tongue movements of speech, food manipulation, and swallowing.