Exam 3 Neuro Flashcards
Describe the pain of a migraine headache
pulsating or throbbing pain
ocular or periorbital icepick-like pains
Usually Lateralized HA
Lasts 4 to 72 hours
Pain is aggravated with routine physical activity.
An aura of transient neurologic symptoms (commonly visual) may precede head pain
Possible causes of a migraine
may be exacerbated by emotional stress, fatigue, foods containing nitrite or tyramine, or the menstrual period.
Besides pain…. what are symptoms of a migraine
Nausea; sensitivity to light, sound, and exertion; and a proclivity to retreat to a dark, quiet room typify migraine
Describe the pain of a tension headache
band-like pain is common with tension headaches
are worse with stress or at the end of the day
non-throbbing, mild to moderate pain severity
duration- 30min - 7days
No impact on activity, uncommon to have associated symptoms, NO aura, triggers- tension and anxiety, 10% more common in females, Fx Hx- unlikely, minimal impact on daily life.
Describe the pain of a cluster headache
ocular or periorbital icepick-like pains
lateralized headache
Typically occur at night and awaken the patient
Pain is severe
NO aura
Usually substantial impact on daily life
Episodes of severe unilateral periorbital (behind right or left eye) pain occur daily for several weeks and are often accompanied by one or more of the following: ipsilateral nasal congestion, rhinorrhea, lacrimation, redness of the eye, and Horner syndrome (ptosis, pupillary meiosis, and facial anhidrosis or hypohidrosis).
When do cluster headaches occur?
tend to occur at the same time each day or night
What mood changes may accompany a cluster headache
Anxiety, agitation, and even suicidality
What type of headache pain suggests a neuritic cause
Sharp lancinating pain
What headache characteristics are typical when a patient has an intracranial mass lesion
dull or steady headache
Typically worse upon awakening
What type of headache pain is characteristic an ophthalmologic disorder?
Ocular or periocular pain
Where is the headache pain associated with trigeminal or glossopharyngeal neuralgia
the pain is localized to one of the divisions of the trigeminal nerve or to the pharynx and external auditory meatus, respectively.
What are the precipitating factors associated with headaches
Recent sinusitis, dental surgery, head injury, or symptoms suggestive of a systemic viral infection may suggest the underlying cause
When is an MRI or CT warranted for a headache?
When a patient has a progressive headache disorder, new onset of headache in middle or later life, headaches that disturb sleep or are related to exertion, and headaches that are associated with neurologic symptoms or a focal neurologic deficit usually require cranial MRI or CT scan to exclude an intracranial mass lesion.
Signs of meningeal irritation and impairment of consciousness also indicate the need for further investigation (cranial CT scan or MRI and examination of the cerebrospinal fluid) to exclude subarachnoid hemorrhage or meningeal infection.
Patho of migraines
neuronal dysfunction in the trigeminal system resulting in release of vasoactive neuropeptides such as calcitonin gene-related peptide leading to neurogenic inflammation, sensitization, and headache. Migraine aura is hypothesized to result from cortical spreading depression, a wave of neuronal and glial depolarization that moves slowly across the cerebral cortex corresponding to the clinical symptoms (ie, occipital cortex and visual aura)
What is a specific aura finding related to familial hemiplegic migraine
attacks of lateralized weakness represent the aura.
What are focal disturbances associated with migraine aura
Visual disturbances occur commonly and may consist of field defects; of luminous visual hallucinations such as stars, sparks, unformed light flashes (photopsia), geometric patterns, or zigzags of light; or of some combination of field defects and luminous hallucinations (scintillating scotomas).
Other focal disturbances such as aphasia or numbness, paresthesias, clumsiness, dysarthria, disequilibrium, or weakness in a circumscribed distribution may also occur.
When a patient has red flag findings like neurologic signs or symptoms, Changes in mental status, Weakness, diplopia, papilledema, and focal neurologic deficits associated with a headache, what are the possible causes?
Encephalitis, subdural hematoma, subarachnoid hemorrhage, intracerebral hemorrhage, tumor, mass, increased ICP
When a patient has red flag findings like a Thunderclap HA that peaks within seconds… what is typically the cause of the headache?
Subarachnoid hemorrhage
When a patient has red flag findings like Progressively worsening HA what are the possible causes?
Secondary HA
When a patient has red flag findings like Cancer or Immunosuppression what are the possible causes of the headache?
Brain infection, metastases, HIV infection, AIDS
When a patient has red flag findings like Meningismus what are the possible causes of the headache?
Meningitis, Subarachnoid hemorrhage, subdural empyema
When a patient has red flag findings like Red eye and halos around lights what are the possible causes of the headache?
Acute angle-closure glaucoma
When a patient has red flag findings like Systemic symptoms (fever, wt loss) what are the possible causes of the headache?
Sepsis, thyrotoxicosis, cancer
When a patient has red flag findings like Onset of HA after ago 50 what are the possible causes of the headache?
Increased risk of serious cause (tumor, giant cell arteritis)
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?
Giant cell arteritis
When a patient has red flag findings like Pulsatile tinnitus what are the possible causes of the headache?
Idiopathic intracranial HTN
What is the pharmacological management for an acute attack from a migraine headache?
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!
Why should opiates be avoided when treating headaches?
They can cause rebound HA and addiction
What are non pharmacological ways to treat migraine headaches
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
What are the preventative therapies for migraines
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
Pharmacological treatment for tension HA
Acetaminophen
ASA
NSAIDs (ibuprofen, ketoprofen, and naproxen) more effective than acetomen.
Ketorolac IM is effective for in-office or inpatient
Nonpharmacologic treatment for tension HA
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!!
Pharmacological treatment for cluster HA
Acute attack: Sumatriptan (Imitrex), Zolmitriptan, DHE 45, Ergotamine tartrate aerosol, 100% OX inhalation - 7L/min for 15 min
Avoid medication oversue!! = analgesic rebound HA
Nonpharmacologic treatment for cluster HA
Lifestyle modification and supportive care- limited benefit d/t unknown precipitating factors
Avoid triggers if known
F/U visits at regular intervals
Prophylactic treatment for cluster HA
Verapamil, 240-480 mg/day
Lithium carbonate, 150-600mg/day
Topiramate, 50-200 mg/day
Valproic acid 500-2000 mg/da
What symptoms are associated with a Basilar artery migraine
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
What symptoms are associated with a Ophthalmoplegic migraine
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.
Precipitants of migraines
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)
Clinical features and symptoms of a brain tumor
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
What is the source of a brain tumor
Can be primary malignancy or secondary (common metastatic sources) Lung, melanoma, renal, and breast, GI tract
How to treat increased ICP associated with a brain tumor
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 patientwith ICP
Treatment for seizures associated with a brain tumor
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)
General symptoms associated with a brain tumor
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
Symptoms associated with Frontal lobe lesions
Progressive intellectual decline, slowing mental activity, personality changes, contralateral grasp reflexes, expressive aphasia
Symptoms associated with Temporal lobe lesions
Seizures, olfactory or gustatory hallucinations. Smacking or licking lips, emotional changes, behavioral changes, visual disturbances.
Symptoms associated with Parietal lobe lesions
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.
Symptoms associated with Brainstem and cerebellar lesions
Cranial nerve palsies, ataxia, nystagmus, sensory deficits in the limbs, and incoordination
What imagining to obtain to rule out brain neoplasm
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
What is the most common primary brain tumor
Glioblastoma multiforme is the most common primary tumor, followed by meningioma and astrocytoma
Treatment of glioblastoma
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
What is dementia
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).
Patho of Alzheimer’s
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.
Alzheimer’s predisposing factors
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
Office or bedside screening toolsfor Alzheimer’s
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
Diagnostic Criteria for the Dementia syndrome associated with lewy body
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
Signs and symptoms of Alzheimer’s
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.
Signs and symptoms of Subcortical Dementia- (dementia of parkinson’s disease & some cases of vascular dementia)
present with psychomotor slowing, reduced attention, early loss of executive function, & personality changes.
Signs and symptoms of Dementia with Lewy bodies
fluctuating cognitive impairment , rigidity, bradykinesia are the primary signs. These pts often have visual hallucinations - typically of people & animals.
Signs and symptoms of Frontotemporal dementia
includes pick disease. Pts manifest with personality changes (euphoria, disinhibition, apathy, & compulsive behaviors.
Diagnostics/labs for dementia
CBC, BMP, calcium, BUN, creatinine, glucose, TSH, & vitamin B12levels, 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)
Non - pharmacological management of dementia
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.
Pharmacological management of dementia
Acetylcholinesterase Inhibitorsegdonepezil, galantamine, rivastigminefor mild to moderate alzheimer’s. These meds may also have benefit in pts with vascular dementia or dementia with lewy bodies.S/En/d, anorexia, weight loss, & syncope
Memantine- specifically beneficial for pts with advanced disease
Symptomatic mgmtof depression, agitation, delusions, hallucinations which may respond to specific medications
Nonpharmacologic tx of insomnia
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
Pharmacological tx of insomnia
Lorazepam- short term use only 1-2 wks
Zolpidem
Temazepam
Antihistamines egbenadryl&hydroxyzine
Atypical antidepressanttrazodone( adv. not habit forming esp. in lower doses)
Causes and predisposing factors of delirium
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
risk factors for Delirium
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)
Onset of delirium
Sudden; days or weeks. Associated with a physical stressor
Onset of dementia
Gradual; months or years
Essential features of delirium
Clouded sensorium, irritability and anxiety, misperception of sensory stimuli, possible hallucinations, lucid periods, alternating with confusion, suspiciousness, agitation
Essential features of dementia
Memory loss, decreased intellectual functioning (confabulation and circumstantiality), loss of executive function
Causes of delirium
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
Causes of dementia
Neurotransmitter deficit, cortical atrophy, ventricular dilation, cerebrovascular accident (multi-infarct dementia), Lewy bodies, Alzheimer’s disease, Parkinson’s disease, Huntington’s chorea
Age for delirium
Any age
Age for dementia
Usually older than 60
CAM screening tool
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
Most common metabolic disorders associated with delirium
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
Treatment of ICU delirium
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
Labs/diagnostics for Giant cell arteritis
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
• Gold standard for diagnosis of Giant cell arteritis
Temporal artery biopsy
Signs and symptoms of Giant cell arteritis
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
Management of Giant cell arteritis
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
Positive Temporal artery biopsy findings for Giant cell arteritis
inflammatory infiltrate in the media and adventitia with lymphocytes, histiocytes, plasma cells, and giant cells
Signs and symptoms of Wernicke’s encephalopathy
characterized by confusion, ataxia, and nystagmus leading to ophthalmoplegia (lateral rectus muscle weakness, conjugate gaze palsies); peripheral neuropathy may also be present.
Causes of Wernicke’s encephalopathy
Itis 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.
Tx of Wernicke’s encephalopathy
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
Multiple Sclerosis patho
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.
Demographics of Multiple Sclerosis
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
Signs and symptoms of Relapsing-remitting Multiple Sclerosis
Most Common
clear defined episodes of relapse and recovery (usual initial presentation)(82%)
Signs and symptoms of Secondary progressive Multiple Sclerosis
-usually initiates with RR-MS followed by deterioration or progression of the disease. Patients usually do not return to baseline, few or no relapses
Signs and symptoms of Primary progressive Multiple Sclerosis
Continued disease progression, some plateaus and minor temporary improvements
Signs and symptoms of Progressive relapsing Multiple Sclerosis
progressive disease from onset with clear relapses. Continued progression of disease between relapses, occurs in 5% of MS patients
Signs and symptoms of Malignant MS
Rapid onset, progressive deterioration, disability and death in short period of time.
Signs and symptoms of Benign MS
No deterioration after 10 years following onset of disease
General Signs and symptoms of Multiple Sclerosis
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
Physical Examination Findings of MS
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.
Labs/diagnostics for MS
Test of choice, CSF Analysis
Neurological Exam
Multiple Foci best visualized by MRI
MRI findings for MS
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.
CSF findings for MS
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
can you make definite diagnosis of MS based on labs?
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)
Treatment for acute exacerbation of MS
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)
Symptomatic Therapy for MS
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.
What is Uhthoffs phenomenon
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
Cause of Myasthenia gravis
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
Signs and symptoms of Myasthenia gravis
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
Labs/diagnostics for Myasthenia gravis
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)
1st line tx for myasthenia gravis
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
2nd line therapy for myasthenia gravis
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
Inpatient management of Myasthenia gravis crisis
Plasmapheresis or IVIGand protect airway
Surgical management of Myasthenia gravis
thymectomy; all MG pts <65 are good candidates and benefit from thymus removal unless weekness is restricted to extraocular muscles
Medications to avoid for Myasthenia gravis
beta-blockers, aminoglycoside and quinolone antibiotics, penicillamine, interferons, class I antiarrhythmics-procainamide, quinidine
Indications for intubation/airway support for Myasthenia gravis
FVC <15-20 ml/kg, max expiratory pressure <40cm h2o, neg inspiratory pressure <25-30 cm h2o, or weak cough effort in crisis
When to admit Myasthenia gravis pts to icu
Exacerbation with respiratory involvement, requiring plasmapheresis can be managed on floor at most facilities
Beside diagnostic test for Myasthenia gravis
(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
What is Lambert-Eaton syndrome
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
Tx of Lambert-Eaton syndrome
treatment with IVIG, plasmapheresis, prednisone, and azathioprine.
What is Guillian-Barre Syndrome
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.
What is the Preceding event for Guillian-Barre Syndrome
Frequent antecedent infections include the following: upper respiratory infections, campylobacter jejuni enteritis, cytomegalovirus infection, epstein barr virus infection, hepatitis infection, HIV and mycoplasma infection
Signs and symptoms of Guillian-Barre Syndrome (there are a lot!)
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.
Guillian-Barre Syndrome prognosis
Most patients will have a good outcome without sequelae after appropriate treatment and management but approximately 5% will die from complications.
How does Guillian-Barre Syndrome affect respiratory status
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.
CSF findings with Guillian-Barre Syndrome
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
CBC findings with Guillian-Barre Syndrome
early leukocytosis may be seen with a left shift that resolve during the course of the illness.
General management of Guillian-Barre Syndrome
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
Pharmacological treatment of Guillian-Barre Syndrome
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
Signs and symptoms of miller Fisher Syndrome
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.
What is Ramsay hunt
a localized herpes zoster infection involving the seventh nerve and geniculate ganglia, resulting in hearing loss, vertigo, and facial nerve palsy.
What are the signs and symptoms of Ramsey hunt
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.
Diagnostic test for Ramsey hunt
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
Management of Ramsey hunt
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.
Referrals for ramsey hunt
Ophthalmology referral if corneal damage/ulceration occurs.
ENT referral if significant nerve impairment or development of synkinesis.
Signs and symptoms of Bell’s palsy
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.
Management of Bell’s palsy
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.
What is trigeminal neuralgia
Trigeminal neuralgia is an intense, usually unilateral paroxysmal, stabbing pain in the sensory distribution of the trigeminal (cranial nerve V) nerve.
What is the etiology of trigeminal neuralgia
-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
Clinical features of trigeminal neuralgia
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
What triggers pain in patients with trigger neuralgia
Touch, an air current, or activities such as shaving, eating or brushing teeth
What to suspect trigeminal neuralgia in patients under the age of 40?
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.
2 major differentials for trigeminal neuralgia and how to rule them out
CT to r/o neoplasm
ESR to r/o temporal arteritis
Pharmacological tx of trigeminal neuralgia
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
Tx of trigeminal neuralgia patients with refractory pain
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
What is ALS
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).
Symptoms and physical findings of ALS
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
Pharmacologic treatment of ALS
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.
What will EMG for ALS show
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.
ALS prognosis
Mean duration of symptoms is 3 – 5 years. Approx 20% of patients survive >5yr.
ALS nonpharmacologic therapy
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
What is Parkinson’s dz
Progressiveneurodegenerative disorder caused by degeneration ofDopaminergicneuronsin the substantia nigra pars compacta.
Symptoms of Parkinson’s
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
Etiology of Parkinson’s
Dopamine depletionin 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
Nonpharmacologic tx of Parkinson’s
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
Pharmacological tx of Parkinson’s
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)
What is status epilepticus
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
Pharmacological tx for status epilepticus
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
Initial management priority for status epilepticus
Initial management is SUPPORTIVE
Maintenance of airway and 50% dextrose (25-50mL) IVF in case hypoglycemia is responsible
Causes of status epilepticus
- 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
What are Focal (Partial) Seizures
cortical discharges localized within one cerebral hemisphere. Focal seizures can involve impairment of consciousness and may evolve to convulsive seizures.
Symptoms of Focal (Partial) Seizures Without impairment of consciousness
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
Symptoms of Focal (Partial) Seizures With impairment of consciousness
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
Describe absence seizures
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
Describe Atypical absence seizures
Alteration in consciousness typically last longer; accompanied by motor signs; less responsive to anticonvulsants; may be accompanied with developmental delay or mental retardation
Describe Myoclonic seizures
consist of single or multiple myoclonic jerks
Describe Tonic-clonic “grand mal” seizures
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)
Describe status epilepticus
a series of seizures lasting longer than 5 min with the patient never returning to baseline between seizures
Describe Atonic seizures
consist of brief (less than 2 seconds) loss of muscle tone and results in fall known as Epileptic drop attack.
Differential diagnosis for focal seizures
- TIA’s- longer duration, lack of spread, and negative symptoms (weakness, or numbness).
- 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).
- 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.
- Rage attacks- situational and lead to goal directed aggressive behavior.
Differential dx for generalized seizures
- Syncope-rapid recovery with recumbency- NO postictal headache or confusion. However in some instances motor accompaniments and urinary incontinence may simulate a seizure.
- Cardiac dz- cerebral hypoperfusion due to cardiac rhythm disturbance should be suspected in patients with episodic LOC.
- Brainstem ischemia- LOC is preceded by other brainstem signs.
- 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
Causes of metabolic seizure activity
Acidosis,
Electrolyte imbalances (hyponatremia, hypocalcemia),
Hypoglycemia,
Hypoxia,
**Alcohol or barbiturate withdrawal are themost commoncauses of new onset seizures in adults
Causes of seizures
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
Diagnostics and labs for seizures
-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)
Therapeutic drug range for phenytoin
Phenytoin (Dilantin)- 10-20 mcg/ml
Therapeutic drug range for phenobarbital
PHenobarbital- 15-30 mcg/ml for epilepsy control
What is a TIA
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.
Etiology of TIA
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.
Recurrence of TIA and risk for stroke
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.
What is a stroke
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
Causes of stroke
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.
What is a Lacunar Infarction
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.
What is a Cerebral infarction
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.
What is an ischemic stroke
Sudden onset of a focal neurologic deficit as a result of a cerebral ischemia resulting in cell death.
Etiology of ischemic stroke
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.
What is a hemorrhagic stroke
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
Predisposing factors of hemorrhagic stroke
HTN, use of anticoagulants or thrombolytics, use of illicit street drugs (cocaine), heavy use of alcohol, hematologic disorders.
Symptoms of ischemic stroke affecting the middle cerebral artery
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).
Symptoms of ischemic stroke affecting the posterior cerebral artery
unilateral hemianopia; blindness with anosognosia (anton syndrome) if bilateral.
Symptoms of ischemic stroke affecting the Posterior inferior cerebellar artery
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.
Symptoms of ischemic stroke affecting the Anterior cerebral artery
hemiplegia {lower extremity more often than upper extremity), primitive reflexes, confusion, abulia, bilateral anterior infarction may cause behavioral changes and disturbance in memory.
Symptoms of ischemic stroke affecting the Vertebral and basilar arteries
decreased LOC, vertigo, N/V, diplopia, quadriparesis or quadriplegia, locked in syndrome, dysphagia, ipsilateral cranial nerve findings, contralateral (or bilateral) sensory and motor deficits.
Symptoms of ischemic stroke affecting the Deep penetrating branches of major cerebral arteries (lacunar infarction)
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.
Symptoms of SAH
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.
Hunt and Hess grading scale for SAH
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
Fisher grading scale for SAH
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.
Symptoms and physical findings of ICH
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)
How to calculate ICH score
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.
Signs and symptoms of obstruction of Anterior cerebral artery
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.
Signs and symptoms of obstruction of Middle cerebral artery
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.
Signs and symptoms of obstruction of Ophthalmic or central retinal artery
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.
Signs and symptoms of obstruction of Posterior cerebral artery
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.
Signs and symptoms of obstruction of Vertebral artery occlusion
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.
Signs and symptoms of obstruction of Posterior inferior cerebellar artery
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.
Signs and symptoms of obstruction of Vertebral or Basilar artery
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.
Signs and symptoms of obstruction of Cerebellar arteries
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.
Lacunar syndrome symptoms
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.
Lacunar syndrome CT findings
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
Management of acute ischemic stroke
Airway and breathing should be maintained
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Supplemental Oxygen should be provided to keep the oxygen saturation >92%
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Pneumatic compression devices or pharmacological means should be applied to help prevent deep venous thrombosis
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Avoid any and all oral intake until swallowing is clearly unimpaired; this helps to prevent aspiration pneumonia
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Early mobilization for rehab is desirable
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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.
thrombolytic therapy for ischemic stroke
IV T-PA, or alteplase, is the only medical therapy approved by the U.S FDA for the treatment of acute ischemic stroke.
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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
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The protocol is weight based with 90mg being the maximum allowable dose.
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The risk of brain hemorrhage with IV t-PA is about 6% in stroke patients
Three-Hour Criteria for Tissue TPA Use in Patients with Thromboembolic Stroke: INCLUSION criteria
• 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
Three-Hour Criteria for TPA Use in Patients with Thromboembolic Stroke: EXCLUSION criteria
• 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
Hypertension in patients with ischemic stroke
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
Hypotension in patients with ischemic stroke
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
Non pharmacological therapy for hemorrhagic stroke
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.
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Surgery should be performed promptly for cases of cerebellar hemorrhage of >3 cm when the patient is deteriorating clinically, showing brainstem edema or hydrocephalus.
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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.
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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.
Acute General Tx of hemorrhagic strokes
The cornerstones of medical management of acute intracerebral hemorrhage include:
Control of hypertension
Correction of coagulopathy
Management of elevated intracranial pressure
Treatment of seizures
Hypertension (BP Control) for hemorrhagic stroke
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.
Suggested Recommended Guidelines for the treatment of Elevated blood Pressure in patients with spontaneous intracerebral hemorrhage
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.
Correction of Coagulopathy of hemorrhagic stroke
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.
Treating Elevated intracranial pressure in patients with hemorrhagic stroke
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.
Treating Seizures in patients with hemorrhagic stroke
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.
Supportive Treatment for patients with hemorrhagic stroke
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
What type of brain bleed can be ruled out with CSF
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.
Percentage of patients with TIAs who will develop stroke
- The 90-day risk of stroke after TIA is 17%
- The greatest risk is within the first week
- Approximately one third of stroke patient have a history of TIA
Imaging workup for a pt with suspected stroke
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.
Lab workup for a pt with suspected stroke
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
Ekg for suspected stroke
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.
Echo for suspected stroke
Echocardiography (with agitated saline contrast) should be performed in cases of nonlacunar stroke to exclude valvular disease, left to right shunting, and cardiac thrombus.
Management of stroke
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.
When to use embolectomy for stroke
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.
Anticoagulant therapy in suspected stroke
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.
Early CT scan findings associated with brain ischemia
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
Hypoattenuatingbrain tissue
Obscuration of the lentiform nucleus
Insular Ribbon sign
Dense MCA sign
Hemorrhagic infarcts
Treatment of cerebral edema
Cerebraledema 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
clinical deterioration findings in patients with hemorrhagic strokes
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
Risk factors for Subarachnoid hemorrhage
Older age
Female sex
“Nonwhite” ethnicity
Hypertension
Tobacco smoking
High ETOH consumption (>150g per week)
Previous symptoms
Posterior circulation aneurysms
Larger aneurysms
When to obtain LP when Subarachnoid hemorrhage is suspected
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
LP findings for Subarachnoid hemorrhage
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
Clinical features of Subarachnoid hemorrhage
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”
CT use for suspected Subarachnoid hemorrhage
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.
Blood pressure goals for Subarachnoid hemorrhage
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
Treatment for vasospasm
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
What is meningitis
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.
Predisposing Factors for Developing meningitis
Sinusitis - otitis media - mastoiditis - pneumonia - trauma - congenital malformations
Drugs causing drug-induced aseptic meningitis
NSAIDS
Sulfonamides
Certain Monoclonal antibodies
What is bacterial meningitis
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.
Patho of bacterial meningitis
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.
Bacterial meningitis: Streptococcus pneumoniae (who does affect signs and symptoms)
(pneumococcal meningitis):most common,most seriousbacterial 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)
Bacterial meningitis: Neisseria meningitidis(meningococcal meningitis) who does it effect, how does it spread
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
Bacterial meningitis: Haemophilus influenzae: who does it affect
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
Bacterial meningitis: Escherichia coli, Enterobacter, Klebsiella, andProteus. who does it affect
May occur, in infants, elderly, immunosuppressed
Aseptic or Viral Meningitis patho
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
Aseptic or Viral Meningitis signs and symptoms
less severe: Fever, Headache, Nuchal rigidity, Photophobia, Myalgias, Vomiting, Rash
Aseptic or Viral Meningitis transmission
through cough, saliva, and fecal matter of an infected person
Aseptic or Viral Meningitis causes
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
Clinical manifestations of bacterial meningitis
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
Brudzinski’s sign
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
Kernig’s sign
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.
Indications for LP in patients with suspected meningitis
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.
Contraindications for LP in patients with suspected meningitis
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
List of Supplies needed for Lumbar puncture
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
CSF abnormalities with bacterial meningitis
Cloudy, elevated opening pressure >180, increased WBCs (100-5000), increased total protein(100-500), decreased glucose (5-40), bacteria present on gram stain
CSF abnormalities with viral meningitis
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
Antimicrobial management of meningitis
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 withhx of neurosurgery or head trauma
Therapy will be Cefepime and Vancomycin
Chemoprophylaxis Therapy of meningitis
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
Medication therapy for meningitis (besides chemo and antibiotics)
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.
Duration of xanthochromia
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.
intracranial abscessessentials for diagnosis
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
intracranial abscesssigns and symptoms
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.
Imaging and labs for intracranial abscess
CT will show area of contrast enhancement surrounding a low density core. Elevated WBCs and sed rate. LP- elevated opening pressure, increase in protein
Tx for intracranial abscess
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
Tx for Neisseria meningitidis (meningococcal)
give Meningococcal Penicillin G q4h, if allergic, give ceftriaxone or cefotaxime
Tx for H. Influenzae meningitis
if beta lactamase negative, give ampicillin;
if beta lactamase positive, give ceftriaxone or cefotaxime
Aseptic meningitis tx
Start empiric therapy, give supportive therapy
Tx for tuberculosis meningitis
give INH, pyridoxine, rifampin, pyrazinamide, and ethambutol along with empiric therapy
Tx for streptococcus pneumoniaemeningitis
add dexamethasone to empiric therapy. Give with FIRST antibiotic dose, NOT after regimen has started.
HSV encephalitis: CT findings
Hemorrhage and edema in TEMPORAL lobes
ABSOLUTE Contraindications for Lumbar Puncture
Infection in the tissues near puncture site–infection may spread to brain.
Midline shift
Posterior Fossa mass
RELATIVE Contraindications for Lumbar Puncture
Increased ICP caused by a space occupying lesion (blood, tumor, orespecially brain abscesses)– LP may cause herniation
Coagulopathy
Severe thrombocytopenia
Caution is advised when doing LP if patient has…
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 havenotbeen shown to increase risk of bleeding following LP.
Pt with prior lumbar fusion or laminectomy
Safety concerns when pressure is reduced in the spinal canal during LP
Cardiorespiratory collapse
Stupor
Seizures
Sudden death
Herniation–particularly in pts with brain abscesses
11 steps for performing lumbar puncture
- Obtain consent.
- Position ptin 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
- ID andmark 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.
- Prep the skin—apply antiseptic solution in circular motion from the center outward, gradually increasing the circumference
- Apply sterile drape—with window open to L4
- Anesthetize—Lidocaine 1% —create a wheal with anesthetic in the skin over the entry site;thenanesthetize the deeper tissues. *Ask about anesthetic allergies.
- 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.
- Visualize CSF—will flow from the needle hub when the subarachnoid space is punctured and the stylet is removed. CSF is normally clear.
- 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.
- 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
- Replace styletbefore 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).
When to obtain a CT scan prior to LP
Patients with altered LOC
Focal neurologic findings
> 60 yo
Immunocompromised pts
Papilledema–seen on PE
If brain occupying lesion is suspected or known (especially abrain 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)
emergency complication of cerebral shunts
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
indications for cerebral shunts
Long-term management of increased ICP
Currently VP shunts are the mainstay for treatment of hydrocephalus–ease of insertion and reliable long-term function
Intracranial shunt malfunction signs/symptoms
Continued enlargement of ventricles – they usually diminish in size after shunt placement in pts withhigh-pressurehydrocephalus (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
Cranial nerves
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): Thisnerve controls the tongue movements of speech, food manipulation, and swallowing.
