FNP III Neuro pII

Two different types of CVA:

Hemorrhagic - most often caused by intracerebral hemorrahage from ruptured aneurysms, AVMs, HTN arteriolar disease and amyloid deposition.

Ischemic- the obstructions that cause ischemic CVAs can be caused by atherosclerosis, embolus, thrombus, hemorrhage, or vasospasm.  Up to 85% are due to ischemia. 

• Modifiable risk factors for CVA include:  
• HTN, cardiac disease, diabetes, hypercholesterolemia, smoking, illicit drug use, and lifestyle factors.

Four fold increase in CVA when BP is >160/95

Five fold increase in CVA when pt. has AFIB.

African Americans 2-3 X greater risk of CVA. 

TIA time line:

A brief bout of ischemia will produce neuro-deficits.  

If ischemia is short lived, neuro signs and symptoms resolve within one hour.

When neurological deficits take more than 4 hours to improve, some neuronal death has probably occurred. 

Epidural hematomas - caused by severe head injury, most common along the temporal cranial wall and result from tears in the middle meningeal ARTERY.  

Leaking arterial blood creates a hematoma between dura and bone increasing ICP and decreasing perfusion.   As the hemotoma increases, it causes CONTRALATERAL hemiparisis and IPSILATERAL oculomotor nerve palsy and enlarged pupil.  Eventually this can lead to herniation and death.

• RIGHT EPIDURAL HEMATOMA
• RIGHT SIDED OCC MOTOR NERVE AND DIALATED PUPIL. 
• LEFT SIDED HEMIPARISIS

Subdural hematomas caused by the brain moving against the skull tearing the superficial cerebral veins. 

VENOUS SUBDURAL HEMATOMAS expand more slowly than ARTERIAL epididural hematomas.  

Sometimes resolve spontaneously. Sometimes expand slowly developing neuro deficits or even death.

In subdural hematoma, headache is the single most common symptom and is more common in older adults.  The headache is generalized and often bi-temporal.

Subarachnoid hemorrage is caused by tears in the arteries running along the subarrachnoid space at the surface of the brain.  CSF circulates through the subarchnoid space as such, a lumbar puncture will produced RBCs when there is a subarchnoid hemorrage. Subarrachnoid hemorrage will produce severe HA, vomitting a drowsiness.

• Intraparenchymal hemorrage:
• Maybe caused by sudden rises in cerebral blood pressure.  
• Most commonly from ruptures of arteries supplying basal ganglia and thalmus.

Neuro symptoms of an intraparenchymal hemorrage will reflect the region of the hematoma.  A basal ganglia intraparenchymal hematoma will produce CONTRALATERAL MOTOR WEAKNESS.

Patients presenting with CVA will usually complain of weakness, numbness, or paralysis of one or both extremities on one side of the body.  They complain of severe headache, have impairment of cognitive abilities, level of consciousness, speech, visual fields, extra ocular muscle functioning, motor functioning, and gait.

Likely findings for ischemic CVA caused by thrombus would show that symptoms begin during the day, occurred gradually, and the patient had periods of improvement between episodes of worsening.

Likely findings for steaming CVA caused by embolus reveals that symptoms began during sleep, occurred abruptly, and have progressed steadily.

Symptoms with a hemorrhagic stroke commonly occur during the day with activity and are abrupt in onset, with LOC possibly worsening after the initial onset.

Other indicators are vomiting, seizures, severe headaches, and focal deficits.  The patient may complain of feeling drowsy and dull.

Carotid theories become audible when the distal lumen is narrowed to approximately 3 mm or less.

The higher the pitch of the bruit, the higher the degree of stenosis.

Carotid endarterectomy should not be considered for symptomatic patients with less than 50% stenosis.

The initial assessment of the patient with possible CVA should include a CBC with platelet count, prothrombin time/partial thromboplastin time, electrolytes, blood urea nitrogen, creatinine, glucose, calcium, magnesium, said rate, EKG, and chest x-ray.

The American Heart Association recommends the use of non-contrast CT of the head in patients with suspected acute CVA.

Hematocrit greater than 60 causes increased viscosity, resulting in decreased perfusion, and can contribute to cerebral ischemia

Ischemic CVA caused by embolus has a high incidence rate in pregnant women.

Carotid dissection appears initially with occipital headache or acute neck pain and is followed by a scheming symptoms of developing a, syncope, and amaurosis fugax (temporary loss of vision in ONE eye).

Unilateral neck pain that is sudden and radiates to the ipsilateral face or eye is usually present the headache is related to cervical manipulation, sustained exertion, or trauma.

A symptom of new onset, progressive headache appears as a major feature in temporal arteritis with some cranial symptoms of the diplopia and mental sluggishness.

A symptoms specific to temporal arteritis is claudication of the muscles of mastication.  The patient complains of pain the draw upon prolonged chewing.  Local tenderness of the affected artery is found.  The practitioner should be alert to the potential complication of blindness.  Diplopia is a common sign seen before visual impairment, once visual impairment occurs however, it can progress quickly to blindness in several hours.

The main principle the management of CVA today is CVA prevention and early recognition and treatment.  Patients with symptoms of a possible stroke require immediate referral to an emergency room for evaluation, CT scanning of the brain, and possible use of thrombolytic therapy.

Initial management of a CVA is focused on maintaining adequate tissue oxygenation.  Incubation and mechanical ventilation are initiated when there is decreased level of consciousness.

ESR may be strongly elevated from 50 to 100 mm.

Intravenous thrombolytic therapy is effective in reducing the neurological deficit and some patients without CT evidence of intracranial hemorrhage if administered within 3 hours after the onset of an ischemic stroke.

The optimal dose of ASA is as follows:

Thromboembolic disorders: 325 to 650 MG once or twice daily.

TIA prophylaxis: 650 MG BID

MI prophylaxis: 81 to 325 mg /day.

The most relevant risk factors uncontrolled hypertension, the use of ASA for prophylaxis in patients with moderate to high risk of CVA or TIA, and the use of anticoagulants in patients with afib.

Headaches may be classified into 4 general categories: muscle contraction headaches (tension); vascular headaches (migraines and cluster headaches); mixed headaches (a combination of muscle contraction and vascular); and traction or inflammatory headaches.

Tension headache presents as a mild to moderate bilateral non-pulsating tightening pain that is not aggravated by routine physical activity.


A migraine headache may last 4 to 72 hours and may or may not be precipitated by an aura.  It is usually of moderate to severe intensity with a pulsating quality, aggravated by routine physical activity, and accompanied by nausea, vomiting, and photophobia.

A cluster headache usually occurs at night in may last from 15 to 180 minutes.  There is usually severe unilateral orbital, super orbital, and/or temporal pain that is accompanied on the same side of the face with sweating, lacremation, nasal congestion, ptosis, rhinorrhea, eyelid edema, and/or conjunctival injection.

A traction or inflammatory headache is an acute new onset headache that is of increasing intensity; this type of headache is a medical emergency as it is symptomatic of a more serious condition such as hemorrhage or infection.

Cluster headaches are sponsored 100% oxygen by mask.

Cluster headaches, another former vascular headaches, are named for their pattern of occurrence; they usually come in groups over a span of several weeks or months then disappear for months or even years.

The occur in middle-aged men and typically cluster on a seasonal basis anywhere from 3 to 18 months between headaches

Migraine headaches produce moderate to severe unilateral pain lasting from 4 hours to 3 days.

These headaches throb, cause nausea, and are made worse by activity and are commonly triggered by alcohol, stress, menstruation, or diet.  Migraine headaches also often have a prodrome period.

Migraines without an aura are known as common migraines where as migraines with an aura are known as classic migraines

Migraine treatment can be divided into 4 methods: nonfarm logic, abortive therapy, pain relief, and prophylactic treatment.

Nonpharmacologic measures include exercise a strict schedule for sleep regular meals, and identifying triggers.

Some patients may require 3 different medications: a triptan as an abortive medication, NSAIDs for rescue medication or breakthrough pain, and daily preventive medicine such as propranolol.

Meningitis is an acute inflammation of the men windshield membranes surrounding the structures of the CNS and/or the CSF.

The common factors shared by all types of meningitis is an abnormality in the number of white blood cells in the CSF.

Purulent forms of acute meningitis are usually caused by 3 types of bacteria:  Neisseria meningitidis, haemophilus influenzae type B and strep pneumonaie.

Seasonal occurrence shows a higher incidence of meningitis in the spring and fall.

Viruses, fungi, and parasites can cause meningitis but the serious meningitides are caused by bacteria.

Objective signs include fever usually greater than 103, with accompanying chills, tachycardia, and tachypnea.  Signs of managerial irritation such as Bruzinski's sign (hip and knee flexion when the neck is flexed) and Kernigs sign (inability to fully extend the legs)  are often present.

Altered level of consciousness is present in may include confusion, progressive lethargy, stupor, and coma.

Electrolytes, especially sodium, are evaluated for common complication of meningitis, this syndrome of inappropriate antidiuretic hormone secretion.

Bacterial infection is indicated by cloudy appearance of CSF, increased CSF pressure greater than 20 mm of H2O, protein levels greater than 15 mg per deciliter; increase neutrophils and reduced CSF glucose as compared to simultaneous serum glucose.

Encephalitis is usually a viral causation, and it is an acute inflammation of brain tissue.  This inflammation causes hyperthermia, altered levels of consciousness and other focal neurologic signs.  Encephalitis has also been called "sleeping sickness".

Mosquitoes can carry arboviruses which can cause encephalitis in academic fashion during warm weather months.

A common presentation of viral encephalitis include alteration in level of consciousness related to parenchymal swelling.  The manifestations are usually progressive from lethargy to coma with the swelling and resultant increased intracranial pressure.

Physical exam may reveal a fever, nuchal rigidity, paralysis, hyperresponsiveness of deep tendon reflexes, and possibly, a viral rash.

A lumbar puncture is essential for the diagnosis.

The differentiating factor to consider encephalitis over meningitis is usually alteration in level of consciousness.  Meningitis has an abrupt onset, and although the condition may show signs of parenchymal damage that are seen in encephalitis (memory difficulties, confusion, hallucinations, dysphagia, seizures, and focal motor/sensory deficits), the signs are usually seen late in the course of the disease as compared to encephalitis in which they are exhibited from the beginning.


A preceding viral illness such as measles or mumps points to encephalitis is occurring as a complication

Viral causation is treated with antiviral agents such as acyclovir.  Antivirals are most effective when used early in the course of illness especially before changes in level of consciousness occur.

An osmotic diuretic such as mannitol is chosen 1st to reduce edema, glucocorticoids such as Decadron may be added if necessary.

Herpes zoster, commonly known as shingles is a viral infection caused by varicella zoster occurring along dermtoma pathways and resulting in a vesticular rash especially in the intercostal areas.

Initially, the patient with herpes zoster may present with unexplained pain.

The pain is described as constant or intermittent with a stabbing quality.  The pain occurs along the involved dermatome, usually 48 to 72 hours before eruption of the classic vesicular skin rash.

When herpes zoster is manifested along the branches of the 5th cranial nerve, herpes  ophthalmicus results.  This condition can cause blindness and requires immediate referral to an ophthalmologist for evaluation and treatment.

The skin lesions usually continue to develop for 3 to 5 days, and the entire disease course usually last 10 to 15 days.

Trigeminal neuralgia also known as tic douloureux is a painful idiopathic disorder of the trigeminal nerve.

The Lansing, sharply cutting pain occurs along one or more of the 3 branches of the trigeminal nerve.  Patients will do almost anything to prevent triggering an episode.

Although it is extremely painful, trigeminal neuralgia produces no obvious neurological deficits.

Trigeminal neuralgia is caused by focal demyelination of axons in the affected nerve, ganglion, or root.

A physical exam the cranial nerves specifically the trigeminal nerve abnormal motor and sensory function and facial muscle strength and reflexes are normal.

 The cardinal signs of idiopathic trigeminal neuralgia are elicited when a facial trigger point is stimulated; the patient experiences a sharp electric type pain that follows the distribution of the trigeminal nerve.

Diagnosis of trigeminal neuralgia is made primarily from clinical history.   A trial treatment of Tegretolthat demonstrates improvement may further confirm the diagnosis.

Tegretol is 1st line pharmacologic therapy for trigeminal neuralgia.

Bell's palsy is a condition with an acute onset of flaccid paralysis, usually occurring on one side of the face in an otherwise healthy person.

The cause is unknown.

Patients with Bell's palsy present with acute onset of partial or total facial paralysis on one side of the face, usually involving lower motor neurons.  The physical assessment reveals absence of forehead wrinkles, wider palpebral fissure of the eye, decreased corneal reflex and Bell's phenomenon.

Bell phenomenons - the eyeball turns upward when the patient tries to close the eyelid.

Bell's palsy can be diagnosed because of its acute onset and the fact that no other CNS symptoms exist.

Diagnosis is made primarily on patient history and clinical examination.

60% of patients with Bell's palsy totally recover without treatment.  Management of a patient with idiopathic Bell's palsy is primarily directed at preventing eye injury.  

Loss of the ability to blink or close the eyelid subjects  the cornea to drying and ulceration.

The patient is instructed to keep the eye moist by using topical application of artificial tears every 30 minutes during the day and the use of an ocular lubricating ointment at night.

GBS is usually an ascending paralysis most often beginning in the legs than progressing in an ascending fashion.

The diagnosis is made by spinal fluid analysis which shows an elevated protein, especially gamma globulin with little or no cellular response.

The treatment involves intravenous gamma globulin or plasmapheresis.

It may progress to chronic form, chronic inflammatory demyelinating polyneuropathy.

Botulism is a rare paralytic bacterial illness that enters through an infected wound or the oral route.  Infection can occur from unpasteurized food and IV drug use.

The bacterium forms and endotoxin that affects nerve endings causing paralysis.

Treatment is primarily preventive, but in acute cases ventilator support may be necessary.

Myasthenia gravis is an autoimmune disorder of the neuromuscular junction where and antibody occupies the muscle receptor for acetylcholine.

It affects smaller muscles which have more acetylcholine receptors the larger muscles.  Therefore eye movements and speech are most commonly affected.

Symptomatic treatment is Mestinon and affords temporary relief.  

For permanent relief of symptoms, antibody suppression is needed.  This may be accomplished through immuno-suppressant drugs.

Plasmapheresis may help also to reduce antibodies.