MR OGUNDELE NERVOUS SYSTEM 3 CRANIAL NERVE CRANIAL

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MR OGUNDELE NERVOUS SYSTEM 3

MR OGUNDELE NERVOUS SYSTEM 3

CRANIAL NERVE

CRANIAL NERVE

CRANIAL NERVE OLFACTORY: Ask the patient to smell perfume or ground coffee. OPTIC :

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,

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.

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 is a chronic neurological disorder characterized by recurrent seizure activity. seizure is the

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

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

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

Generalized seizures Tonic clonic Begins with tonic (stiffening/rigidity of muscles of limbs), micturition, salivation

Generalized seizures Tonic clonic Begins with tonic (stiffening/rigidity of muscles of limbs), micturition, salivation and tongue-biting may occur loss of consciousness, then clonic (rhythmic jerking) Tonic Stiffening or rigidity of muscles; increased tone, respiration ceases loss of consciousness Clonic Rhythmic jerking of muscle contraction and relaxation Brief loss of conscious awareness and staring into space; appears to be daydreaming Brief stiffening or jerking of extremity, Sudden shock-like jerks affecting one part or the whole body Absence Myoclonic Atonic Loss of muscle tone causing patient to fall to

Partial seizures Simple partial Begins with aura; may have unilateral unusual sensation or movement

Partial seizures Simple partial Begins with aura; may have unilateral unusual sensation or movement of extremity, autonomic (heart rate, flushing), or psychic changes; no loss of consciousness Complex partial Loss of consciousness; automatisms (lip smacking picking, patting)

Diagnostic test An EEG is the most useful test for evaluating seizures CT scan

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

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

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

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

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 is a medical emergency, This is defined as a prolonged single attack

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.

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

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

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

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

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

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

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

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

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 acute replace with or without recovery.

DIAGNOSIS No laboratory diagnosis can establish a diagnosis of MS MRI brain and spinal

DIAGNOSIS No laboratory diagnosis can establish a diagnosis of MS MRI brain and spinal cord shows increased intensity lesions CSF shows oligoclonal bands of Ig. G 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,

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 relapsingremitting. Avonex may reduce exacerbations and delay disability.

MANAGEMENT The progressive forms of the disease are more difficult to treat, and immunosuppressive

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 parasympathetic agents such bethanechol (Urecholine). with as

Nursing Management Monitor movements for interference with activity of daily living. Encourage activity balanced

Nursing Management Monitor 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

Nursing Management Educate and train the client on Bladder training. Educate client on Medication compliance Provide psychological support.

Myasthenia gravis (MG) means “grave muscle weakness, ” or weakness of the voluntary or

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

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

PATHOPHYSIOLOGY Receptors on the muscle tissue take up ACh and contraction of the muscle results. In MG. antibodies prevents the acetylcholine from binding to the receptor sites on the skeletal muscle, inhibiting normal muscle contraction in the affected area.

Myasthenia gravis

Myasthenia gravis

PATHOPHYSIOLOGY At the neuromuscular junction, immune complexes are deposited at the postsynaptic membrane causing

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

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 characteristic feature. single most Ptosis (drooping of the eyelid) due

S/S Fatiguability is the characteristic feature. single most 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

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

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 pyridostigmine treat

MANAGEMENT No cure has been found for MG. Oral anticholinesterases such as pyridostigmine treat 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 Plasmapheresis and intravenous immunoglobulin are usually reserved for severe acute exacerbations. Thymectomy (surgical

MANAGEMENT Plasmapheresis and 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

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

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

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,

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

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.

BELL’S PALSY

BELL’S PALSY

S/S Unilateral facial paralysis—inability to close eye, wrinkle forehead, puff out cheeks, or smile.

S/S Unilateral facial paralysis—inability to close eye, wrinkle forehead, puff out cheeks, or smile. Pain near the ear and jaw Altered taste

DIAGNOSIS History of the onset of symptoms is used to diagnose Bell’s palsy Electromyogram

DIAGNOSIS History of the onset of symptoms is used to diagnose Bell’s palsy Electromyogram (EMG) used to indicate recovery time; can determine prognosis

MANAGEMENT Administer corticosteroids over 7 to 10 days to decrease edema/inflammation. Analgesics are given

MANAGEMENT Administer corticosteroids over 7 to 10 days to decrease edema/inflammation. Analgesics are given for pain control. Antiviral medication may be prescribed Moist heat with gentle massage to the face and ear also eases pain. Administer artificial tears to maintain moisture within eyes.

NURSING MANAGEMENT Administer pain medication as prescribed. Monitor for visual changes—dryness of eye can

NURSING MANAGEMENT Administer pain medication as prescribed. Monitor for visual changes—dryness of eye can lead to irritation of cornea. Monitor patient for reaction to medications Teach patient on proper instillation of artificial tear drops.

Trigeminal neuralgia is a relatively rare facial pain syndrome.

Trigeminal neuralgia is a relatively rare facial pain syndrome.

PATHOPHYSIOLOGY Trigeminal neuralgia is a condition of the fifth cranial nerve characterized by paroxysms

PATHOPHYSIOLOGY Trigeminal neuralgia is a condition of the fifth cranial nerve characterized by paroxysms of pain in the area innervated by any of the three branches, It emerges as two roots (large sensory and small motor root) and gives off 3 branches: ophthalmic (V 1), maxillary (V 2) and mandibular (V 3).

TRIGEMINAL NERVE

TRIGEMINAL NERVE

PATHOPHYSIOLOGY The cause is not certain, but chronic compression or irritation of the trigeminal

PATHOPHYSIOLOGY The cause is not certain, but chronic compression or irritation of the trigeminal nerve or degenerative changes to initiate onset of symptoms In most cases ophthalmic nerve is not involve, This can lead to Complete loss of sensation on one side of the face

CAUSES Unknown Risk factor includes: pressure on the nerve root by tumor or blood

CAUSES Unknown Risk factor includes: pressure on the nerve root by tumor or blood vessel leison. MS can also be a factor

S/S The most notable symptoms is severe facial pain The earliest sign is loss

S/S The most notable symptoms is severe facial pain The earliest sign is loss of the corneal reflex. Dissociated sensory loss (i. e. loss of pain but touch intact) NB. If touch is lost, but pain and temperature intact, the lesion has to be in the pons or medulla. lower jaw deviates to the side of the lesion when the mouth is opened, Frequent blinking and tearing of the eye on the affected side also occurs

DIAGNOSIS History of observation diagnosis. symptoms and direct of an attack confirm Radiological studies,

DIAGNOSIS History of observation diagnosis. symptoms and direct of an attack confirm Radiological studies, (CT scan and MRI, )may be used to rule out other causes of the pain.

MANAGEMENT Anticonvulsant ( carbamazepine, phenytoin) is prescribed to relieve spasmodic pain Severe pain can

MANAGEMENT Anticonvulsant ( carbamazepine, phenytoin) is prescribed to relieve spasmodic pain Severe pain can be relieved by injecting glycerol into the terminal branch of trigeminal nerve (glycerolrhizotomy) Surgical options are available if there is no relief with medication. Surgery is done to identify and remove the cause of irritation and inflammation of the nerve

Parkinson disease is named after James Parkinson who described the syndrome in 1871. It

Parkinson disease is named after James Parkinson who described the syndrome in 1871. It is a degenerative disease that is neurological in nature. It is sometimes called shaking palsy

Parkinson disease Parkinson’s disease is a chronic degenerative movement disorder that arises in the

Parkinson disease Parkinson’s disease is a chronic degenerative movement disorder that arises in the basal ganglia in the cerebrum. PD is a disorder of the extra pyramidal system, in particular the motor structure of the basal ganglia.

Parkinson disease This is the part of the brain that controls balance and coordination.

Parkinson disease This is the part of the brain that controls balance and coordination. The basal ganglia are gray matter that is scattered throughout the white matter of the cerebrum. Stimulation of the basal ganglia causes muscle tone in the body to be inhibited and promote refined voluntary movements.

Parkinson disease Acetycholine producing neurons transmit excitatory messages throughout the basal ganglia while dopamine

Parkinson disease Acetycholine producing neurons transmit excitatory messages throughout the basal ganglia while dopamine inhibit the function of these neurons so there can be control of voluntary movement. The substantia nigra is a group of cells located within the basal ganglia, which is situated deep within the brain. These cells are responsible for the production of dopamine.

Parkinson disease Parkinson’s disease is caused by destruction of the cells of the substantia

Parkinson disease Parkinson’s disease is caused by destruction of the cells of the substantia nigra, resulting in decreased dopamine production. Therefore, the acetycholine secreting neuron remain active results in the tremor, muscle rigidity, and akinesia (loss of muscle movement) characteristic of Parkinson’s disease.

Etiology The etiology of Parkinson’s disease is unknown

Etiology The etiology of Parkinson’s disease is unknown

Sign and symptoms A triad ofsymptoms are characteristic of PD: tremor, bradykinesia (slow movement)

Sign and symptoms A triad ofsymptoms are characteristic of PD: tremor, bradykinesia (slow movement) and rigidity. Tremor: occurs when the body is at rest, decrease when there is voluntary movement and absent when patient sleep.

Bradykinesia Bradykinesia: patient has poor body balance, difficulty initiating movement, foot may drag or

Bradykinesia Bradykinesia: patient has poor body balance, difficulty initiating movement, foot may drag or may be stiff, bent forward posture when walking. Rigidity: affects the skeletal muscles and contributes to postural changes. Postrural change affects coordination and balance. Speech becomes low in tone, monotonous sounding, drooling may occur. The patient may experience constipation, incontinence, heat intolerance, and decreased sexual ability.

Diagnosis The characteristic features of the disease are used to diagnose the disorder MRI

Diagnosis The characteristic features of the disease are used to diagnose the disorder MRI scan of the brain may be performed to rule out other neurological disorder Positron emission tomography can display reduced uptake of dopamine.

Management There is no cure for Parkinson’s disease. Care is individualized for each patient

Management There is no cure for Parkinson’s disease. Care is individualized for each patient based on presenting symptoms

Management Antiparkinsonian Medications: Administer antiparkinsonian agents which are able to cross the blood-brain barrier.

Management Antiparkinsonian Medications: Administer antiparkinsonian agents which are able to cross the blood-brain barrier. These drugs absorb better on an empty stomach: Levodopa is converted to dopamine in the basal ganglia, producing symptom relief. e, g levodopa, carbidopa-levodopa

Management Dopamine Agonists: Administer dopamine receptor agonists to act directly on the dopamine receptor

Management Dopamine Agonists: Administer dopamine receptor agonists to act directly on the dopamine receptor sites: e. g bromocriptine • Monoamine Oxidase Inhibitors (MAO Inhibitors): Administer selegiline, a selective monoamine oxidase , inhibitor that inhibits dopamine breakdown and is thought to slow the progression of the disease

NURSING MANAGEMENT Monitor neurological status for changes. Monitor respiratory status for changes. Encourage self-care,

NURSING MANAGEMENT Monitor neurological status for changes. Monitor respiratory status for changes. Encourage self-care, allow patient extra time. Encourage exercise; assist with passive ROM if necessary. Educate and encourage patient on medication compliance. Provide psychological support.

HUNTINGTON’S DISEASE Is a rare genetically transmitted degenerative neurological disorder characterised by abnormal movement.

HUNTINGTON’S DISEASE Is a rare genetically transmitted degenerative neurological disorder characterised by abnormal movement. Simply put it is a genetically inherited progressive chorea and dementia.

Causes Huntington’s disease is an autosomal dominant condition (offspring of an affected parent has

Causes Huntington’s disease is an autosomal dominant condition (offspring of an affected parent has a 50% chance of inheriting the disorder). It is genetically transmission by abnormal gene on the short arm of chromosome 4 and it is accompanied by a decline in intellectual capacity and emotional disturbance.

PATHOPHYSIOLOGY This is a degenerative disease that presents with a gradual onset of involuntary,

PATHOPHYSIOLOGY This is a degenerative disease that presents with a gradual onset of involuntary, jerking movements (chorea) and a progressive decline in mental ability, resulting in behavioral changes and dementia. It is uncertain what caused the mutation of the gene responsible for Huntington’s disease.

PATHOPHYSIOLOGY Structurally the disease is characterized by degeneration of the corpus striatum, caudate nucleus,

PATHOPHYSIOLOGY Structurally the disease is characterized by degeneration of the corpus striatum, caudate nucleus, ( these basal ganglia nuclei are important in control of movement) and other deep nuclei of the brain and portions of the cerebral cortex. There are neurochemical effects, such as a depletion of acetylcholine and GABA but an increase in somatostatin and other hormones in the striatum. This results in a loss of inhibition of the dopaminergic pathway, i. e. release of dopamine which leads to chorea The person progress from a state of fidget and restless to a state of constant movement.

S/S Personality changes Irritability or moodiness Psychiatric disturbance Progressive dementia as disease causes further

S/S Personality changes Irritability or moodiness Psychiatric disturbance Progressive dementia as disease causes further neurologic degeneration

S/S Restlessness or fidgeting due to dyskinesia Abnormal, jerking movements (chorea) Depression Paranoia is

S/S Restlessness or fidgeting due to dyskinesia Abnormal, jerking movements (chorea) Depression Paranoia is common,

DIAGNOSIS Genetic testing can detect gene presence even prior to onset of symptoms. CT

DIAGNOSIS Genetic testing can detect gene presence even prior to onset of symptoms. CT scan shows cerebral atrophy later in disease. MRI shows atrophy later in disease.

MANAGEMENT No definite treatment cures the diseases Dopamine-blocking drugs such as haloperidol and dopamine-depleting

MANAGEMENT No definite treatment cures the diseases Dopamine-blocking drugs such as haloperidol and dopamine-depleting drugs such as tetrabenazine may help to control the chorea. Patients and their families should be offered genetic testing and counselling where appropriate.

NURSING MANAGEMENT Provide basic needs for the patient, assist with ADLs as needed. Protect

NURSING MANAGEMENT Provide basic needs for the patient, assist with ADLs as needed. Protect the patient from suicide attempts due to depression. Assist the patient with positioning for safety and comfort. Advocate for genetic counseling for family members of patients Provide psychological support.