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Learn about cranial nerve function assessment, epilepsy overview, types of seizures, diagnostic tests, treatment options, nursing management, and an introduction to multiple sclerosis.
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MR OGUNDELE NERVOUS SYSTEM 3
CRANIAL NERVE • OLFACTORY: Ask the patient to smell perfume or ground coffee. • OPTIC : Test Visual acuity with a Snellen chart • OCCULOMOTOR: Assess pupil size, shape and equality. Test pupilary reflex with pen touch. • TROCHLEAR : Same as occulomotor, ask patient to follow hand as you move it. • TRIGEMINAL: Open jaw against resistance, corneal reflex tested, sensation of pain, touch and temperature tested.
CRANIAL NERVE • ABDUCEN: Test Similar to CN III • FACIAL: Ask pt to smile, frown, raise eye brow, puff out cheeks. • VESTIBULOCOCHLEA: Whisper from distance and ask from pt what you said. Test bone conduction with turning fork. • GLOSSOPHARYNGEAL: Position of Uvula checked, Gag and swallowing reflex check. Ask the patient to Cough. Ask the patient to say Ah!
CRANIAL NERVE • VAGUS: Position of the uvula is checked, gag and swallow reflex checked. • SPINAL ACCESORY: Stenocleidomastoid and trapezius checked for strength by asking person to rotate head and shrug shoulder against resistance. • HYPOGLOSSAL: Ask pt. To protrude and retract tongue, to move it sideways
Epilepsy • Epilepsy is a chronic neurological disorder characterized by recurrent seizure activity. seizure is the sudden, uncontrolled discharge of brain neurons, which produces changes in motor or autonomic function, consciousness, or sensation. • Epilepsy may be acquired or idiopathic (unknown cause). Causes of acquired epilepsy include traumatic brain injury and anoxic events
Epilepsy • Messages from the body are carried by the neurons (nerve cells) of the brain by means of discharges of electrochemical energy that sweep along them. • Sometimes, cells may continue to firing after a task is finished. And this may cause part of the body supplied by such nerve cell to perform erratically. • This leads to mild to incapacitating and often causes unconsciousness when these uncontrolled, abnormal discharges occur repeatedly, a person is said to have an epileptic syndrome .
Partial and generalized seizure Partial seizures • In focal epilepsy (partial seizures), paroxysmal discharges develop in one part of the cerebral hemispheres, the temporal lobe being the most common site Generalized seizures • Paroxysmal discharges are generated in deep sites at the hypothalamic, thalamic or upper brainstem level, and spread rapidly to both hemispheres simultaneously to produce generalized epileptic discharges
Diagnostic test • An EEG is the most useful test for evaluating seizures • CT scan • MRI
NB • Prior to the seizure, the patient may experience an aura, a sensory alteration involving sight, sound, or smell. After the seizure, the patient enters a post-ictal stage where there may be confusion and the patient is often fatigued.
TX • The patient with a primary seizure disorder will typically be managed with anticonvulsant medications. Some patients will need multi-drug regimens to adequately control the seizure disorder. • Administer anticonvulsant medications: carbamazepine, phenytoin, phenobarbital • Surgery is indicated for patients whose epilepsy results from intracranial tumors, abscess, cysts, or vascular anomalies.
Nursing management • Monitor patient during the seizure for breathing, skin color • Monitor patients need for supplemental oxygen post-seizure. • Monitor duration of seizure and progression of symptoms. • Monitor for incontinence of bladder or bowel. • Position patient to decrease risk of injury
Nursing management • Remove objects that may injure patient. • Turn patient on side to reduce risk of aspiration. • Do not insert anything in patient’s mouth during seizure. • Assess the patient post-seizure.
Status epilepticus • Status epilepticus is a medical emergency, This is defined as a prolonged single attack or continuing attacks of epilepsy without intervals of consciousness for at least 30 minutes. MGT • General measures include airway protection, oxygen and intravenous access. • Give i.v. glucose . • Lorazepam or diazepam are first-line treatment • If no response, intravenous phenytoin loading dose of 15 mg/kg is given.
Multiple Sclerosis (MS) • MS is a chronic inflammatory disease causing demyelination in the CNS. • An immune-mediated disease characterized by discrete areas of demyelination in the brain and spinal cord.
Causes • It is thought that there is an abnormal immune response, possibly triggered by an unknown viral antigen. • Genetic predisposition to the disease
Pathophysiology • This is an autoimmune disease that results in demyelination of the CNS • It is a neuromuscular disorder that involves disruption of the transmission of impulses between neurons and the muscles that they stimulate.
Pathophysiology • Myelin is the protective sheath around the axon that transmit electrical impulses from one neuron to the next and act as a thick protective insulator. • In multiple sclerosis, the myelin sheath begins to break down (degenerate) as a result of the activation of the body’s immune system.
Pathophysiology • The nerve becomes inflamed and edematous, myelin becomes eroded by inflammation and replaced by scar tissue and this affect transmission of nerve impulse. • Nerve impulses to the muscles slow down. As the disease progresses, Nerve impulses become completely blocked causing permanent loss of muscle function in that area of the body.
S/S MS affects many systems of the body. Symptoms have periods of exacerbation and remission. • Motor dysfunction: weakness or paralysis of the limb, neck, diplopia caused by oculomotor weakness • Sensory dysfunction: numbness, tingling, burning, painful sensation, hearing loss and Lhermitte's sign (electric shock sensation down the spine when neck is flexed)
S/S • Coordination problem: ataxia, tremor, slurred speech, dysphagia • Mental changes: depression, impaired judgment, memory loss • Fatigue • Urinary urgency or hesitancy due to changes in sphincter control
Clinical features There are several patterns of the course of MS. • Relapsing-remitting MS (most common) affecting different areas of the CNS at different times, with full or partial recovery between episodes, but no progression between. • Primary-progressive MS: the pattern is that of chronic progressive deterioration from the time of onset.
Clinical features • Secondary-progressive MS: there is initial onset of relapsing-remitting, followed by a steady worsening course and may not have occasional relapse. • Relapsing progressive MS: disease worsening from onset, there are acute replace with or without recovery.
DIAGNOSIS No laboratory diagnosis can establish a diagnosis of MS • MRI brain and spinal cord shows increased intensity lesions • CSF shows oligoclonal bands of IgG only within the CNS • Disease history, signs and symptoms experienced by the patient assist with diagnosis
MANAGEMENT MS has no cure. Supportive management and counselling, physiotherapy as indicated. • Short course, high-dose oral or intravenous steroids are used in acute relapses. Are given to decrease inflammation and edema of the neuron, which may relieve some symptoms. • β interferon has been used in clearly relapsing-remitting. Avonexmay reduce exacerbations and delay disability .
MANAGEMENT • The progressive forms of the disease are more difficult to treat, and immunosuppressive drugs (cyclophosphamide) may be given to depress the immune system • Bladder problems are treated with parasympathetic agents such as bethanechol (Urecholine).
Nursing Management • Monitor motor movements for interference with activity of daily living. • Encourage activity balanced with rest periods. • Assess and monitor cognitive function for changes, or deterioration
Nursing Management • Educate and train the client on Bladder training. • Educate client on Medication compliance • Provide psychological support.
Myasthenia gravis • Myasthenia gravis (MG) means “grave muscle weakness,” or weakness of the voluntary or skeletal muscles of the body.
PATHOPHYSIOLOGY • This is a disorder of the peripheral nervous system whereby antibodies bind to receptor sites that normally bind acetylcholine. • Normally, at the neuromuscular junction, the neuron releases the chemical neurotransmitter acetylcholine (ACh), which crosses the synaptic cleft.
PATHOPHYSIOLOGY • Receptors on the muscle tissue take up ACh and contraction of the muscle results. • In MG. antibodiesprevents the acetylcholine from binding to the receptor sites on the skeletal muscle, inhibiting normal muscle contraction in the affected area.
PATHOPHYSIOLOGY • At the neuromuscular junction, immune complexes are deposited at the postsynaptic membrane causing interference with and later destruction of the acetylcholine receptor. • The areas of the body most commonly affected by the autoimmune disease include the muscles in the eyes, face, lips, tongue, throat, and neck, resulting in weakness and fatigue of these areas.
CAUSES No specific cause has been found for MG • There also appear to be genetic factors • Disorders of the thymus gland are often associated with MG (The thymus appears to be involved in the pathogenesis, with 25% of cases having a thymoma and a further 70% have thymic hyperplasia)
S/S • Fatiguability is the single most characteristic feature. • Ptosis (drooping of the eyelid) due to muscular weakness • Diplopia (double vision) due to inability to keep both eyes focused on the same object • Difficulty swallowing (dysphagia) due to muscle weakness
S/S • Weakness of the facial muscles will result in a bland facial expression. • Laryngeal involvement produces dysphonia (voice impairment) and increases the patient’s risk for choking and aspiration
DIAGNOSIS • Edrophonium (anticholinesterase) – Tensilon test – injected i.v. as a test dose provides improvement within seconds lasting for 2–3 minutes • Electromyography (EMG) shows reduced muscle response to repeated stimulations. • CT scan to rule out thymoma. • A simple test involves the patient looking upward for 2 to 3 minutes. Increased droop of the eyelids (ptosis) occurs if MG is present.
MANAGEMENT • No cure has been found for MG. • Oral anticholinesterases such as pyridostigminetreat the weakness but do not affect the course of the disease. (NB: Remember that ACh causes muscles to contract. If ACh is allowed more time to attach to muscle tissue receptors, the muscle contracts and strength is increased) • Corticosteroids can be used with good results in 70% despite risk of an initial relapse.
MANAGEMENT • Plasmapheresisand intravenous immunoglobulin are usually reserved for severe acute exacerbations. • Thymectomy (surgical removal of thymus gland) for patients with thymoma • Avoid aminoglycoside antibiotics which may exacerbate symptoms
NURSING MANAGEMENT • Encourage frequent rest periods. • Monitor vital signs. • Monitor nutritional intake. • Monitor neurologic status for changes in pupil reaction, extraocular movements, eyelid movement, facial symmetry, hand grip strength, coordination, fine motor skills, and gait.
NURSING MANAGEMENT • Monitor respiratory status for changes in rate, effort, skin color, use of accessory muscles, or change in mental status. • Avoid heat extremes • Avoid Alcohol as it may exacerbate symptoms.
BELL’S PALSY • Bell’s palsy (facial paralysis) refers to idiopathic weakness of the muscles of facial expression.
PATHOPHYSIOLOGY • BELL’S PALSY (BP) is due to unilateral inflammation of the seventh cranial nerve, which results in weakness or paralysis of the facial muscles on the affected side • The cause is thought to be nerve trauma from a viral or bacterial infection, the disorder is more common in diabetic patients.
PATHOPHYSIOLOGY • Loss of motor control generally occurs on one side of the face, making the patient unable to close the eyelid, raise the eyebrow, or smile on the affected side of the face. • Some patients will experience pain around the ear on the affected side. The patient may have an associated change in taste.
S/S • Unilateral facial paralysis—inability to close eye, wrinkle forehead, puff out cheeks, or smile. • Pain near the ear and jaw • Altered taste