barone neuro 2012 final.ppt - mycme

9/28/2012

UMDNJ Review Course 1

Physician Assistant Board ReviewDean Barone MPAS, PA-C, AT-C

UMDNJ PANCE/PANRE Review Course

56%

A. 5-15B 10 25


A. B. C. D.

19%

0%

25%

B. 10-25C. Too manyD. Not enough

There are 360 questions on the PANCE and 300 on PANRE Approximately 6% of the questions are neurological Approximately 21 questions on PANCE and 18 questions

on PANRE The NCCPA “blueprint” was followed in the development

of this talk The information is not always what is used in current

practice, all information comes from Cecil Textbook of Medicine, 23rd ed., or Current Medical Diagnosis & Treatment, 2010

Review of sample test from multiple publications on average there were 20 questions 25% stroke (5), 25% headache (5), 20% seizure (4), 10% Alzheimer's (2), 20% miscellaneous (4)


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60%

A. left carotid artery ischemic stroke

A. B. C. D.

32%

4%4%

strokeB. basil artery

stenosisC. right carotid TIAD. subarachnoid

hemorrhage


Transient loss of consciousness and postural tone from inadequate cerebral blood flow with spontaneous, prompt recovery without resuscitative measures

Caused from cardiac abnormality (rhythm or y ( yhemodynamic), vascular disorder or neurologic process.

Work up includes cardiac, vascular and neurologic work up.

Treatment is based on findings of work up.


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Focal ischemia causing neurologic deficit/s lasting <24 hrs.


Embolism- Cardiac from RA, infective endocarditis, atrial myxoma,

mural thrombus, atrial septal defects- Atherosclerosis

Vascular abnormality (less common)y ( )- Fibromuscular dysplasia- Inflammatory disorders

- Giant cell arteritis- SLE- Polyarteritis- Syphilis- Subdural steal syndrome


Subclavian Steal Syndrome

Hematological causesSickle cell- Sickle cell

- Hyperviscosity syndrome- Severe anemia


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Public domain pictures found at:◦ http;//en.wikipedia.org/wiki/Anterior_cerebral_ar

tery

Depends on area of brain affected:

•Public domain pictures found at:–http;//en.wikipedia.org/wiki/Anterior_cerebral_artery (top left)–http://en.wikipedia.org/wiki/Internal_capsule(bottom left)–http://en.wikipedia.org/wiki/Parietal_lobe(right)

Carotid-weakness contralateral body-numbness or paresthesia-dysphoniavisual loss non ocular (ipsilateral to-visual loss non-ocular (ipsilateral to lesion)

-reflex changes


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Public domain pictures found at: (respectively)◦ http;//en.wikipedia.org/wiki/Anterior_cerebral_artery◦ http;//en.wikipedia.org/wiki/Stroke


Middle Cerebral Artery◦ main trunk◦ contralateral hemiplegia◦ eye deviation toward the side◦ contralateral hemianopsiap◦ contralateral hemianesthesia


Middle Cerebral Artery Trunk occlusion of dominant hemisphere causes

aphasia where as non-dominant causes perception deficits (anosognosia)

Superior division occlusion causes contralateral deficits of arm and face with sparing of leg and ffoot

Inferior division occlusion of the dominant side causes Wernicke’s aphasia and non-dominant side causes visual neglect of contralateral side

Inferior division occlusion of either side causes superior quadrantanopsia or homonymous hemianopsia


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Public domain pictures found at:◦ http;//en.wikipedia.org/wiki/Anterior_cerebral_artery


Anterior Circulation◦ Mental status impairment Confusion, amnesia Perseveration Personality change (flat affect, apathy) Cognitive change (short attention span, slowness) Deterioration of intellectual function

◦ Urinary continenceContralateral hemiparesis or hemiplegia◦ Contralateral hemiparesis or hemiplegia

◦ Sensory impairment (contralateral)◦ Foot and leg deficits More frequent than arm deficits Footdrop

◦ Apraxia on affected side◦ Expressive aphasia (left side)◦ Deviation of eyes and head to the affected side◦ Abulia Inability to make decisions voluntary acts

◦ Gait dysfunction


Public domain pictures found at:◦ http;//en.wikipedia.org/wiki/Anterior_cerebral_artery


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The major PCA stroke syndromes comprise the following:

Paramedian thalamic infarction Visual field loss Visual agnosia Balint syndrome Balint syndrome Prosopagnosia Palinopsia, micropsia, and macropsia Disorders of reading Disorders of color vision Memory impairment Motor dysfunction


Public domain picture found at:◦ http;//en.wikipedia.org/wiki/Anterior_cerebral_artery


Vertebrobasilar-Vertigo-Ataxia-Diplopia-Dysarthria-Blurred vision-Perioral weakness-Drop attacks-Bilateral weakness


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Public domain picture found at:◦ http;//en.wikipedia.org/wiki/Stroke Barone personal file image


Public domain pictures found at:◦ http;//en.wikipedia.org/wiki/Broca’s_area


General Recovery Guidelines◦ 10 percent of stroke survivors recover almost completely◦ 25 percent recover with minor impairments◦ 40 percent experience moderate to severe impairments

requiring special care◦ 10 percent require care in a nursing home or other long-term

care facilitycare facility◦ 15 percent die shortly after the stroke

Rehabilitation◦ Rehabilitation actually starts in the hospital as soon as possible

after the stroke. In patients who are stable, rehabilitation may begin within two days after the stroke has occurred, and should be continued as necessary after release from the hospital.


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89%

A. MRIB. CT scan


A. B. C. D.

5% 5%0%

C. X-rayD. Carotid doppler

- CT- MRI / MRA head & neck- UltrasoundUltrasound


- CBC, Chem- Fasting blood glucose- Peripheral vascular evaluation

ECG- ECG- CXR- Blood culture- Holter monitoring


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-Seizures-Classic migraine

TIA Differential Diagnosis


- Surgery for focal carotid stenosis >30% <98%- If poor operative candidate medical treatment

- If underlying disease, treat the disease- Heart embolization

h i th C di (if t

TIA Treatment

- heparin then Coumadin (if not contraindicated)

- Vascular system embolization- aspirin- ticlopidine (Ticlid)


Focal ischemia or cerebral hemorrhage causing neurologic deficit/s >24 hrs.

Same symptoms, imaging and lab studies as TIA

Treatment: if no hematoma is present.1. heparin then Coumadin2. Thrombolytic therapy (if meets criteria)

1. Contraindications: BP >185/110, recent surgery, recent hemorrhage, administration anticoagulants, arterial puncture at non-compressible site, symptoms greater than 3 hours.

3. Steroid and hyperosmotic medications if marked brain edema is present


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Blister of a blood vessel from genetic malformation of the arterial wall or environmental factors causing change in wall architecture.

Most common cause of subarachnoid hemorrhage.

Usually occur at the bifurcation of the vasculature.


When unruptured it may cause local neurological deficits from compression◦ PCOM causes a painful ipsilateral third nerve palsy

Rupture will cause an immediate significant headache associated with LOC and/or nausea and vomiting

Common description “worst headache of my life” or “thunder clap” with immediate headachethunder clap with immediate headache

Usually have neck pain and increased pain with neck movement

May have neurological deficits if bleed damages the parenchyma

May have significant increased intracranial pressure or hydrocephalus from obstruction of ventricular pathway


Patients may complain of recent headaches for approximately 2 weeks

Patients may complain of photophobia or phonophobia

Meningismus is Kernig's sign (flexed hip Meningismus is Kernig s sign (flexed hip results in hamstring pain on leg straightening) and/or Brudzinski’s sign (flex neck and hips flex in response) positive

Ocular hemorrhage on fundoscopic exam


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CT scan is sensitive in 95% of cases If CT negative, lumbar puncture is

performed. If either is positive then cerebral angiogram

i f dis performed EKG performed to rule out myocardial

infarction from catecholamine/sympathetic changes during initial hemorrhage

Pre-op labs


Depends on location, position, age, current neurologic and medical condition

Craniotomy for clipping of aneurysm (surgery) vs. GDC coiling (interventional)

After aneurysm is protected patient is After aneurysm is protected patient is treated with hypertension, hypervolemia, and hemodilution

If hydrocephalus occurs, an external ventricular drain is placed


89%

a. propranololb. amitriptyline

a. b. c. d.

7%1%3%

b a t pty ec. nifedipined. sumatriptan


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81%A. cluster headacheB classic migraine

A. B. C. D.

0%

16%

3%

B. classic migraineC. tension headacheD. subarachnoid

hemorrhage


96%A. migraineB. subarachnoid

hemorrhage

A. B. C. D.

3% 0%1%

hemorrhageC. cluster headacheD. tension headache


Not fully understood:Changes in brain and scalp blood flow occur with a related dilation pulsation of branches of the external carotid artery

However other literature states it is unclear whetherHowever other literature states it is unclear whether vasodilatation (general) and vasoconstriction (focal neurologic deficits) are a cause or effect

Possible serotonin release resulting in trigeminovasculardysfunction causing a release of substance P and inflammatory process, or activation of the dorsal raphenucleus.


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There are different types of migraines; this is general information.

May have a familial history Attacks may be triggered from emotional or

physical stress, lack or excess sleep,physical stress, lack or excess sleep, missed meals, specific foods, ETOH, menstruation, or use of oral contraceptive

Other triggers include insomnia, barometric pressure change and hunger.


Usually start in adolescence or early adult life

Classic is lateralized throbbing headache Most◦ Lateralize or general

Dull or throbbing◦ Dull or throbbing◦ Anorexia◦ Nausea and vomiting◦ Photophobia◦ Phonophobia◦ Blurred vision


Prodromal period of depression, irritability, restlessness, or anorexia.May be associated with an aura (classic migraine) in 10-20% of patients.

Aura usually precedes the headache by no more than one◦ Aura usually precedes the headache by no more than one hour.

◦ An aura is a transient, reversible neurological visual, somatosensory, motor, or language deficit.

Symptoms usually follow a pattern in each patient, except unilateral headaches may not always occur on the same side.


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History and Physical Diagnosis is based in the symptom patterns

when there is no evidence of intracranial pathology.


Prophylaxis◦ Beta-blockers, calcium channel blockers, tricyclic

antidepressants, or anticonvulsants.Abortive drugs (per Current Medicine) Keep in mind there are many more medications

ergotamine tartrate/caffeine (Cafergot)◦ ergotamine tartrate/caffeine (Cafergot)◦ sumatriptan (Imitrex)◦ zolmitriptan (Zomig)

Analgesics should be used sparingly, can cause rebound headache with dose escalation ◦NSAIDs are probably best for mild to moderate headaches◦opioids should be avoided.


Severe, unilateral, periorbital headache Occurs mostly in middle-age men Occurs daily for several weeks and then goes

into remission. Usually accompanied by one or more of the Usually accompanied by one or more of the

following◦ Ipsilateral nasal congestion◦ Rhinorrhea◦ Lacrimation◦ Redness of eye◦ Horner’s syndrome


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Triggers◦ ETOH◦ Stress◦ Glare◦ Ingestion of specific foods

Cluster HeadachesCluster Headaches

◦ Ingestion of specific foods

Diagnosis◦ Symptoms and exclusion of intracranial

pathology


Treatment◦ Oxygen◦ Medications are subcutaneous or inhaled sumatriptan (Imitrex)

dihydroergotamine (Migranal) dihydroergotamine (Migranal) butorphanol (Stadol)


Generalized headache described as band-like or vice-like pain

Associated with poor concentration neck and back of the head pain, never focal neurologic deficitsdeficits

Exacerbated by emotional stress, fatigue, noise or glare


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Diagnosis is symptomatic, if persists evaluate for intracranial or cervical pathology

Treatment◦ Simple analgesics◦ Anti-migraine medicationAnti migraine medication◦ Massage or hot baths


Migraine◦ Female, unilateral, painful, throbbing, nausea,

photophobia, Cluster◦ Men unilateral occurring daily for period of time◦ Men, unilateral, occurring daily for period of time

then remission Tension◦ Neck and head pain, stress, band-like or vice-like


50%

43%A. tonic clonic seizureB. partial complex

i

A. B. C. D.

4%3%

seizureC. absence seizuresD. partial simple

seizure


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Idiopathic or constitutional◦ Start 5-20 y.o.◦ No cause identified

Symptomatic epilepsy◦ Pediatric

C i l l

Seizures Etiology

Congenital anomaly Perinatal injury

Metabolic◦ ETOH withdrawal◦ Uremia◦ Hypo- or hyperglycemia


◦ Trauma◦ Tumors or space occupying lesion◦ Vascular disease◦ Degenerative disorders Alzheimer's◦ Infectious disease HIV / AIDS related infectious disease Meningitis Herpes Syphilis Cysticercosis


Partial seizures◦ Simple: remain conscious, isolated tonic or

clonic activity of a limb, transient altered sensory perception, if extends to the entire side of body is Jacksonian Marchs de o body s Jac so a a c◦ Complex: characterized by aura of

transient abnormality of sensation, perception, emotion, or memory, loss of consciousness, nausea, vomiting, focal sensory perception, focal tonic or clonic activity, may be accompanied by complex seizures.


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Generalized seizures◦ Absence (petit mal) Pt in conversation misses words, usually unaware of

incidence Mild clonic, tonic or atonic components Impaired consciousness Begin in childhood Stop by age 18 Can progress to other types of seizures


Generalized seizures◦ Atypical absence Marked change in tone Gradual onset and termination Gradual onset and termination◦ Myoclonic Single or multiple myoclonic jerks


Generalized seizures◦ Tonic-clonic (grand mal) Sudden loss of consciousness Rigidness - falls to ground Respiratory onset <1mm Jerking of musculature 2 3mm Jerking of musculature 2-3mm Flaccid coma then consciousness then sleep Status epilepticus – further convulsion with consciousness Serial seizure – consciousness then seizure◦ Atonic Drop attacks


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CBC Blood glucose Liver and renal function CT scan MRI

EEG EEG◦ General (absence) generalized spikes with associated

slow waves◦ Simple partial focal rhythmic discharge at start of

seizure, may have no ictal activity◦ Complex partial interictal spikes or spikes associated

with slow waves in temporal or fronto-temporal areas


Generalized tonic clonic or partial focal seizures- phenytoin (Dilantin)- carbamazipine (Tegretol)- valproic acid (Depakote)- phenobarbital - primidone (Mysoline)- felbamate (Felbatol)- gabapentin (Neurontin)- lamotrigine (Lamictal)- topiramate (Topamax)- oxcarbazepine (Trileptal)- levetiracetem (Keppra)- zonisamide (Zonegran)- tiagabine (Gabitril)


Absence seizures- ethosuximide - valproic acid (Depakote)- clonazepam (Klonopin)

Myoclonic seizuresMyoclonic seizures- valproic acid (Depakote)- clonazepam (Klonopin)


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Can cause permanent brain damage secondary to hyperthermia, circulatory collapse, or excitotoxic neuronal damage

Treat ABC’sM h th i Manage hyperthermia

Break with lorazepam (Ativan) or diazapam (Valium), give phenytoin (Dilantin)


Most common cause of chronic dementia (60-80%)

Steady progressive memory loss and impairment of cognition

Usual onset in 6th or 7th decadeWords associated with this disease are:Words associated with this disease are:◦ Intracellular neurofibrillary tangles (beta-

amyloid tau protein)◦ Extracellular neuritic plaques (senile

plaques)


1. Loss of recent memory2. Inability to learn and retain new information3. Language problems (especially word finding)4. Mood swings5. Personality changesy g6. Progressive difficulty performing activities of daily living7. Abstract thinking or proper judgment may be

diminished8. May respond to loss of control in memory with

irritability, hostility, and agitation9. Some have isolated aphasia or visuospatial difficulties


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1. Patients become unable to learn and recall new information

2. Remote memory is affected but not totally lost 3 Require assistance with activities of daily living3. Require assistance with activities of daily living 4. May wander, be agitated, hostile, uncooperative,

or be physically aggressive 5. Lose all sense of time and place 6. Often get lost and are at increased risk for falls or

accidents secondary to confusion


1. Unable to walk or perform any activity of daily living and are usually totally incontinent

2. Recent and remote memory is totally lost 3 May be unable to swallow and eat and are at risk3. May be unable to swallow and eat and are at risk

for malnutrition, pneumonia, and pressure sores 4. Should be placed in a long-term care facility 5. Eventually they become mute


1. Coma2. Death, usually from infection


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H&P, lab tests, and the exclusion of other causes of dementia.CBC, electrolytes, SMA, thyroid function, B12, folate, VDRL, UA

Folstein Mini-Mental Status ExaminationBarthel scale for activities of daily living85% of patients with AD can be diagnosed with thorough H&P and standard neurologic examIf H&P suggests a mass, a CT or MRI should be done

Depression, the most common psychiatric problem in the elderly, can closely mimic early-stage AD (pseudodementia) and coexists in about 20% of cases -- therefore should be ruled out


Drugs enhance cholinergic neurotransmissionAricept (donepezil)Cognex (tacrine)Exelon (rivastigmine)R d ( l i )Razadyne (galantamine)

Antioxidants, estrogen therapy, and NSAIDs are under studyAvoid drugs that may cause confusion –especially anticholinergic drugs


Inflammatory process thought to be from immunologic disorder

Patients have relapsing-remitting pattern with chronic progressive course

Words associated with MS Words associated with MS◦ Multifocal demylination of white matter◦ Women > men◦ Mid 30’s◦ Relapse-remitting and progressive


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Most common presenting symptoms are: paresthesias in one or more extremities, in the

trunk, or on one side of the face weakness or clumsiness of a leg or hand visual disturbances (dimness of vision, double

vision, or scotomas) Also common are minor gait disturbances,

difficulty with bladder control, vertigo, and mild emotional disturbances

Excess heat may accentuate symptoms and signs.


Indirect, by deduction from clinical and lab featuresMRI with and without gadolinium

shows plaquesCSF b litiCSF abnormalities

IgG greater than 13%,lymphocytes increasedprotein increasedoligoclonal bandsmyelin basic protein may be elevated


Corticosteroids are the main form of treatmentInterferon-B reduces frequency and relapses and may delay eventual disabilityIV gamma globulins may help control relapses

l dRegular exercise to improve conditioning, even in advanced diseaseDrugs for spasticity like baclofenDrugs for painful sensory symptoms include amitriptyline, carbamazepine, and narcotic analgesicsAvoid overwork, fatigue, and exposure to excess heat


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46%a. anti-cholinergics

a. b. c. d.

12%9%

33%

gb. dopaminergicsc. beta blockerd. anti-seizure

medications


Cause unknown or maybe autosomal dominant

Begins at any age Emotional stress enhances symptoms

ETOH i t ( ll t ) ETOH improves symptoms (small amounts) Interferes with manual skills


Tremor ◦ one or both hands◦ the head◦ both hands and the head◦ spares the legsp g◦ speech may be affected


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Medications◦ propranolol◦ primidone if propranolol fails

Surgery◦ ThalamotomyThalamotomy◦ Deep brain stimulator


Occurs in all ethnic groups Equal sex distribution Occurs usually between 45-65 years of age


Primary Parkinson’s Disease◦ Dopaminergic cells are lost in the

nigrostriatal system Causes imbalance between the dopamine

and acetylcholine in the corpus striatumand acetylcholine in the corpus striatum


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Resting, pill-rolling, tremorRigidity and no tremorFace becomes mask-likeMovement becomes slow and difficult to initiatePosture becomes stoopedDiffi l i i i i lkiDifficulty initiating walkingGait becomes shufflingMonotonous, stuttering dysarthriaDementia affects 50% and depression is commonLead-pipe and cogwheel-like rigidity


Early signs include:1. infrequent blinking2. lack of facial expression3. decreased movement4. impaired postural reflexesp p5. characteristic gait abnormalitiesTremor occurs initially in 70% of patientsRigidity occurs but is occasionally minimal or

lacking


Dopaminergics- 1st line◦ levodopa with co-administration of carbidopa, improve

bradykinesia, rigidity, and tremor◦ amantadine is useful in treating early, mild Parkinsonism

and in augmenting the effects of levodopa◦ bromocriptine and pergolide are ergot alkaloids that

directly activate dopamine receptors in the basil gangliaselegiline inhibits the break down of dopamine in the◦ selegiline, inhibits the break down of dopamine in the brain

Anticholinergics- 2nd line◦ Help with tremor and rigidity more than bradykinesia

Remaining as physically active as possible is important.


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Inherited autosomal dominant disorder◦ Chromosome 4 affected The caudate nucleus atrophies, GABA and

Substance P decreaseSubstance P decrease

◦ Develops after age 30

◦ Both sexes affected equally


Develops insidiouslyDementia or psychiatric disturbances; may precede the

movement disorderMotor manifestations include:

1. flicking movements of the extremities2. lilting gait3. motor impersistence (inability to sustain a motor act)4. facial grimacing5. ataxia6. dystonia.

Disorder is progressive - Patients ultimately lose physical and mental abilities to care for themselves


No cureGenetic counselingMedications for symptoms only◦ haloperidol (Haldol) <dyskinesia>◦ haloperidol (Haldol) <dyskinesia>◦ tetrabenazine (Xenazine) <dyskinesia>◦ clozapine (Clozaril) <behavior disturbance>


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Blockage of neuromuscular transmission at the acetylcholine receptors

Most common in young women

Can occur at any agey g

Autoimmune disease can be associated with the following diseases as well:◦ thymic tumor◦ thyrotoxicosis◦ rheumatoid arthritis◦ SLE


Most common symptoms:ptosisdiplopiamuscle fatigability after exercise

Later symptoms include:d h idysarthriadysphagiaproximal limb weaknessquadriparesis/plegiarespiratory distress

Ocular myasthenia gravis involves only extraocularmuscles


Edrophonium or neostigmine administration will cause improvement of symptoms

Electrophysiology testing Serum levels of acetylcholine receptor

antibodiesantibodies


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pyridostigmine (Mestinon) or neostigmine

corticosteroids are useful for long-term treatmenttreatment.

plasmapheresis relieves symptoms.

treatment of associated diseases if present


Unilateral facial muscle weakness without evidence of neurologic disease or apparent cause.

Can be associated with the below:◦ Herpes zoster◦ Lyme disease

C◦ Cancer◦ DM◦ Sarcoid◦ Trauma◦ Cholesteatoma◦ Viral infection


Acute onset (few hours) Unilateral May be pain in or behind the ipsilateral ear

prior to facial weakness

Bell’s Palsy Signs and Symptoms

May have:◦ taste impairment◦ lacrimation impairment◦ hyperacusis


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Clinical diagnosis Evaluated for the associated disease

processes

BellBell’’s Palsy s Palsy DiagnosisDiagnosis


Most resolve spontaneously Oral prednisone with acyclovir if begun soon

after onset improves the percentage of those who recover completely


Idiopathic acute or subacute polyradiculoneuropathy

Following infection, immunization or surgical procedure

Associated with campylobacter jejuni enteritis Associated with campylobacter jejuni enteritis


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Symmetrical lower extremity weakness Proximal greater than distal DTR decreased or absent Sensation may be decreased Autonomic dysfunction◦ Tachycardia◦ Tachycardia◦ Labile blood pressure◦ Sweating◦ Impaired pulmonary function◦ Sphincter decrease◦ Paralytic ileus

Significant affects on the respiratory muscles


Electrophysiology◦ Slowing of the motor and sensory NCV

CSF◦ Elevated proteins◦ Normal cell countNormal cell count


Hospitalization◦ Cardiorespiratory support

Plasmapheresis◦ Improves prognosis, morbidity and mortality

Intravenous immunoglobulin◦ Preferred instead of plasmapheresis if

cardiovascular instability or in children


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Mixed polyneuropathy in majority of cases (70%), the remainder are sensory

Can affect any peripheral nerve including the cranial nerves

O f th lt f l Occurs from the result of vascular insufficiency or nerve infarct associated with hyperglycemia


Most common in lower extremities◦ Numbness◦ Pain◦ Dysesthesia◦ Paresthesia

Patient may have decreased DTR or vibratory sense prior to neuropathyprior to neuropathy

Autonomic complications◦ Postural hypotension◦ Cardiac arrhythmias◦ Impaired thermoregulatory sweating◦ Bowel, bladder , sexual and gastric dysfunction


Serial NCV Labs to rule out other causes of

polyneuropathy◦ Uremia◦ ETOH and nutritional deficits◦ Connective tissue disease◦ Connective tissue disease◦ Vasculitis◦ Vitamin B12 deficiency◦ Hypothyroidism◦ Amyloidosis


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Tight control of serum glucose Drugs to prevent stabbing pain◦ phenytoin (Dilantin)◦ mexiletine (Mexitil)◦ carbamazepine (Tegretol)

Control of deep aching pain◦ amitriptyline (Elavil)p y ( )◦ fluphenazine (Prolixin)

Postural hypotension treatment◦ NaCl◦ TED stockings◦ Medications fludrocortisones midodrine (Proamatine)


Causes vary with age of patient◦ Neonates Escherichia coli◦ Infants Streptococcus◦ Children (6) Haemophilus influenzae

Ad l N i i i itidi◦ Adolescence Neisseria meningitidis◦ Adults Streptococcus pneumoniae


Symptoms are typically acute and caused by: ◦ inflammation◦ increased intracranial pressure◦ tissue necrosis

Fever Headache Vomiting Stiff neck


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CT LP◦ Turbid or purulent◦ Increase pressure◦ WBC elevated (1000 10 000) with neutrophils◦ WBC elevated (1000-10,000) with neutrophils◦ Protien high◦ Glucose low◦ Gram stain usually positive


Empiric antibiotics for symptoms with turbid CSF◦ Neonates ampicillin and gentamicin◦ Infants (3 mo) increase the gentamicin◦ Up to 18 3rd gen cephalosporin or

ampicillin and chloramphenicol◦ Adults IV pen G or ampicillin◦ Elderly ampicillin and 3rd gen

cephalosporin◦ Post op 3rd gen cephalosporin and

nafcillin


Viral meningitis is associated with enteric viruses, coxsackievirus A or B, echovirus, and mumps

Viral encephalitis may not have identifiable cause but associated with childhoodcause but associated with childhood exanthems, arthropod borne agents, herpes simplex 1

Aseptic meningitis may reflect an inflammatory process of parameningeal area


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Acute confusion May have systemic manifestations◦ Rash◦ Pharyngitis◦ Adenopathy◦ Pleuritis

Carditis◦ Carditis◦ Jaundice◦ Organomegaly◦ Diarrhea

Encephalitis◦ Seizures◦ Altered consciousness◦ Focal neurological signs


CT Serum labs normal CSF◦ Normal pressure◦ Cells◦ Cells Increase in lymphocytes or monocytes

◦ Protien and glucose normal


acyclovir if herpes 1 is present acetaminophen (Tylenol) for headache anticonvulsants for seizures

th i th i t t t otherwise there is no treatment


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Umbrella term for non-progressive, non-contagious condition causing physical disability in human development

75% occurs during pregnancy, 5% during g p g y gchildbirth, 15% occurs up to age of 3 with no specific known cause (may be from asphyxia, hypoxia or infection)


Diagnosis is made from history and physical If there is no known cause then MRI is test of

choice and used only for timing of injury Pt with CP may be mentally retarded or have

normal to high IQnormal to high IQ


Treatment is symptomatic to help with muscular contractures and pain associated with muscles or sequelae of arthritis◦ PT/OT to develop motor skills as much as

possible


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Feature Delirium DementiaOnset Rapid Insidious

Duration Hours to days (transient) Months to years (persistent)

Attention Decreased (distractible, fluctuating)

Usually normal (in mild to moderate dementia)

Awareness Always impaired Usually normal

Alertness Fluctuates Usually normal

Consciousness Depressed NormalConsciousness Depressed Normal

Memory Impaired (varies) Impaired (remote better than recent)

Language Normal or incorrect naming Aphasia, anomia, paraphasia

Perceptions Misperceptions, illusions, hallucinations (common)

Usually normal (possibly delusions)

Psychomotor activity Varies (can be increased or decreased)

Usually normal

Sleep-wake pattern Disrupted Normal or fragmented

Physiologic injury only - not an anatomic injury

Different grading systems Post concussion symptoms include

headache, tennitus, concentration difficulty, dizziness

Return to play guidelines simply put: ◦ no symptoms at rest or with exertion for first

time concussion


53%

A. B. C. D.

8%

27%

12%

A. CT scanB. MRIC. lumbar punctureD. basic metabolic

panel


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94%1. cluster headache

t i h d h

1 2 3 4

0% 0%6%

2. tension headache3. migraine

headache4. subarachnoid

hemorrhage


82%

a. narcotic medications

b. beta blockersc. massage or hot

b h

a. b. c. d.

1% 3%

14%

bathd. calcium channel

blockers


57%a. vertigob. ataxiac. dysarthriad. numbness and

a. b. c. d.

13%

28%

3%

paresthesias


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54%

a. CT scanb. MRIc. lumbar

a. b. c. d.

1%

31%

14%

punctured. Kernig’s and

Brudzinski’s maneuvers


100%

a. Diabetes mellitus

a. b. c. d.

0% 0%0%

a abetes e tusb. Hypertensionc. Alzheimer’s

diseased. Huntington’s

chorea


61%

a. Dilantin (hydantoin)

b. Valium

a. b. c. d.

3%3%

34%

(diazepam)c. Keppra

(levetiracetam)d. Tegretol

(carbamazepine)


9/28/2012


87%A. obtain dilantin level

A. B. C. D.

3% 0%

10%

levelB. order CT scanC. check ABC’sD. order immediate

EEG


barone neuro 2012 final.ppt - mycme

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