Nursing Assessment in the Clinical Setting - Volume 2 - The Neurological System

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This may later cause severe pain with further fever, occasional delirium and meningism due to accompanying encephalitis , and a rapid onset of muscle atrophy, fasciculations, and weakness that may be localized or diffuse, mild or profound, and that may be fatal if the respiratory or bulbar muscles are involved.

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Only supportive treatment is available for poliomyelitis, but some recovery occurs in the majority of patients who survive the acute stage of the illness. Since the advent of immunization programs in the s, this disease has been rare in the Western world. Hereditary motor neuropathies also known as spinal muscular atrophies and as Werdnig-Hoffman or Kugelberg-Welander diseases are a diverse group of genetic disorders in which signs of ventral-horn disease occur in babies or young people.

The usual symptoms of muscle atrophy and weakness progress more slowly if the disease begins at a later age 5 to 15 years ; at later ages the disease may also pass, leaving only chronic mild weakness and secondary skeletal deformities such as scoliosis rotation of the spine. Less commonly, muscle weakness occurs in specific patterns—for example, involving only the facial, shoulder, or calf muscles—and the progress of the disease is much slower.

Babies with these disorders may exhibit respiratory insufficiency, poor ability to suck, and severe limpness and weakness of all muscles except those of the face and eyes; the muscles of the shoulder and pelvic girdles are primarily affected. Motor development is delayed or absent.

Diagnosis of hereditary motor neuropathy is confirmed by electromyography and muscle biopsy. Enzyme deficiencies are the cause of some cases of hereditary motor neuropathy, but in most cases the etiological basis of the disease is unknown. Amyotrophic lateral sclerosis ALS and lateral sclerosis are both motor neuron diseases, progressive disorders of older people that affect neurons of the ventral horns, of the medullary motor nuclei, and of the corticospinal tracts. ALS, or Lou Gehrig disease, is characterized by muscle wasting due to loss of the ventral-horn cells the lower motor neurons.

Lateral sclerosis is the loss of axons in the lateral columns of the spinal cord the upper motor neurons of the corticospinal tracts. A combination of upper and lower motor neuron signs is associated with these diseases, but muscle weakness and atrophy of two or more limbs is the primary feature. The brain, eyes, and sensory system are unaffected. Nerve injuries function as neuronal neuropathies affecting the axon far from the cell body.

Injuries are of three main grades of severity. In neurapraxia there is temporary blockage of impulse conduction, although the axons remain intact. More severe stretch or incision damage interrupts some axons and is called axonotmesis. Injury that actually severs the nerve is called neurotmesis; surgical reattachment of the severed nerve ends is necessary. Neurosurgery does not guarantee a rapid recovery, since new nerve sprouts grow down the nerve framework at the rate of 1 to 2 mm 0. Demyelinating neuropathies are those in which the Schwann cells , which form myelin the white, insulating sheath on the axon of many nerve fibres , are primarily affected and migrate away from the nerve.

This process causes the insulating myelin of axon segments to be lost, and conduction of nerve impulses down the axon is blocked.

Acquired demyelinating neuropathies may arise as complications of diphtheria and diabetes , which, partly because of damage to the smallest blood vessels supplying the nerves, are sometimes accompanied by a variety of motor, sensory, autonomic, or mixed neuropathies. Some of these are extremely painful.

Leprosy probably the most common cause of neuropathy in the world , metabolic diseases, cancer , and myeloma or other dysproteinemias also cause demyelinating neuropathies. Charcot-Marie-Tooth disease also known as peroneal muscular atrophy because of the special involvement of shin muscles is a genetically acquired demyelinating neuropathy. High foot arches, distal motor weakness and atrophy, and reduced reflexes are the main symptoms; sometimes the nerves are greatly thickened.

The condition first appears in childhood, though patients have a normal life span. In this disease an autoimmune attack upon the myelin sheath of the motor nerves leads to progressive weakness and reflex loss with only slight sensory changes. Weakness rarely may become so severe that the patient needs mechanical help in breathing , but if further complications do not occur, the disease will remit within a few weeks.

In severe cases, blood transfusion may speed recovery. Carpal tunnel syndrome is a common ischemic neuropathy in which the median nerve is compressed at the wrist. Ischemic neuropathies are those disorders in which nerve compression leads to decreased blood supply and subsequent damage to the Schwann cells.

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The nerve narrows at the site of pressure, although the axon remains intact. Carpal tunnel syndrome causes pain, numbness, tingling, and weakness of the fingers and thumb, especially at night and in the morning. Cubital tunnel syndrome is a similar problem affecting the ulnar nerve at the elbow. Surgical intervention may be necessary to release the entrapped nerve. Damage to the sympathetic or parasympathetic pathways in the hypothalamus or brainstem may produce similar symptoms—for example, faintness due to disordered regulation of blood pressure and heart rate, disturbances of bladder and bowel control, impotence, and impaired visual accommodation.

Some relief may be obtained from medications that replace a deficient neurotransmitter, increase the blood volume, or compress the limbs so that blood no longer pools in the veins. Myasthenia gravis is the most common disease of the neuromuscular junction. At this site the motor nerve impulse normally triggers the release of the neurotransmitter acetylcholine , which diffuses across the synaptic gap between the terminal of the nerve and the specialized end-plate region of the muscle-fibre membrane. In myasthenia gravis, receptors in the end-plate region are partially coated with an antibody, so that the acetylcholine molecules are blocked, depolarization of the muscle fibre cannot occur, and the muscle cannot contract.

The amount of acetylcholine released from the nerve terminal is also reduced. As a result, muscle contraction is possible after a period of rest, but sustained contractions quickly weaken. This fatigability is especially present in the eye muscles, causing drooping of the lids on looking upward and to diplopia double vision. The muscles of the throat, limbs, and respiration may also be involved. Myasthenia gravis is diagnosed by electrical studies of neuromuscular transmission and by single-fibre electromyography see above Neurological examination: Diagnostic tests and procedures.

Treatment involves the removal of the thymus gland which may produce the antibody and medications that augment the effect of acetylcholine and suppress the immune system. Duchenne muscular dystrophy DMD is one of the most common genetic dystrophies. DMD is an X-linked disorder that ordinarily affects only males.

By the age of three the individual experiences difficulty in walking; progressive failure to run, jump, and climb occurs later, leading eventually to the inability to walk. Because of the infiltration of degenerating muscles with fat, little atrophy may be noticed until late in the course of the disease. Diagnosis is confirmed by testing the blood levels of creatine kinase, an enzyme released from degenerating muscle, and also by electromyography and muscle biopsy.

The cause is unknown, and no specific treatment is available, but genetic testing is used to determine whether a case represents a new mutation or has been genetically transmitted by a carrier mother to her son. Facioscapulohumeral dystrophy causes weakness and wasting of predominantly the face, shoulder girdle, and arms in teenagers. Other limb-girdle dystrophies also show slower progression and may not declare themselves until adult life. Oculopharyngeal dystrophies first strike the eye muscles, causing drooping of the eyelids and weakness or paralysis of the muscles moving the eyes.

Later involvement of the face, bulbar muscles, limbs, and trunk is common. Myotonic dystrophy is characterized by weakness and wasting of the face and trunk muscles. In addition, muscles fail to relax after a strong contraction, so that, for example, the patient cannot easily let go after shaking hands. Involvement of other body systems is common.

The same failure of relaxation occurs in myotonia congenita but without the wasting features of myotonic dystrophy. Relaxation can be obtained with medications such as diphenylhydantoin and quinine. Congenital myopathies cause weakness and poor muscle development in the early years of life, but generally they are not progressive. Diagnosis is determined by muscle biopsy. Lipid storage myopathies are associated with disorders of the metabolism of carnitine , a substance that muscle cells use to convert fatty acids into energy.

In these conditions severe muscle weakness progresses slowly. A muscle biopsy shows accumulation of fat in the fibres. In the glycogen storage diseases glycogen accumulates in muscle fibre, because of a deficiency of an enzyme that helps degrade glycogen into lactic acid for the production of energy. Beginning in childhood, fatigue, pain, and occasional severe muscle cramps during exercise are common.

Diagnosis is determined by demonstrating that the exercising muscles do not produce lactic acid as they should. Myoglobinuria is a condition in which myoglobin , a substance that stores oxygen within the muscles, spills into the blood and urine. Myoglobin may accumulate in the tubules of the kidney and cause renal failure.

This condition, which primarily occurs as a result of muscle damage, can also occur as an inherited metabolic defect or may follow heavy exercise, injury, or toxic damage from drugs or chemicals. Malignant hyperthermia is a metabolic muscle disease characterized by high fever and extreme rigidity of muscles, usually caused by certain anesthetics or muscle-relaxant medications given during surgery. Rapid cooling of the patient, correction of the accumulation of lactic acid in the blood the result of intense muscle contraction , and administration of dantrolene sodium to relax the muscles is necessary for treatment.

In familial periodic paralyses episodes of weakness occur in association with abnormally high or low blood levels of potassium. Some attacks are caused by a period of rest following heavy exercise, others are caused by carbohydrate or alcohol consumption.

Neurological Assessment and GCS

Depending on the type of paralysis, treatment includes the administration of potassium, glucose, and diuretics. Myositis , an inflammatory muscle disease, is associated with some viral infections, causing swelling, pain, and weakness, and with trichinosis and other tapeworm infestations, in which allergic skin rashes commonly accompany the same symptoms. Dermatomyositis is an autoimmune disease characterized by swelling, weakness, and tenderness of the proximal, facial, neck, and bulbar muscles in both children and adults.

A skin rash is also present, mainly around the eyes but also on the face and limbs. Diagnosis is determined by electromyography, blood enzyme levels, and sometimes muscle biopsy. Treatment includes steroid and immunosuppressant medications. Closely related conditions without the rash are associated with collagen-vascular diseases, such as scleroderma and polyarteritis, or with cancer. Polymyalgia rheumatica , another autoimmune disease, mainly affects women over the age of Symptoms include severe muscle stiffness especially after sleep , malaise , weight loss, muscle tenderness, anemia, and fever.

Inflammation of arteries, particularly of the branches of the carotids, may also occur. Blindness may follow if the ophthalmic arteries are involved. Treatment with steroid medications produces relief. Spinocerebellar degenerations are genetically determined conditions characterized by dysfunction of the dorsal columns or of the corticospinal and spinocerebellar tracts of the spinal cord. These conditions usually appear in the first 20 years of life and cause position sensation, gait, limb power, balance, and coordination disturbances.

For further discussion, see below The cerebellum: Genetic diseases. Myelitis, inflammation of the spinal cord, may be caused by viral or bacterial infections such as mononucleosis , mumps , measles , chicken pox , tuberculosis , and herpes zoster. Symptoms result from the degeneration of the dorsal roots and include a painful girdlelike sensation around the trunk, a loss of motor, sensory, and bladder functions below the level of the inflammation, meningism, and fever.

Damage to the spinal cord may result from spinal fractures or dislocations. The severity of damage varies with the severity of the injury. Transient weakness and hyperactive reflexes may occur because of damage to the corticospinal tracts, or paraplegia may occur because of damage to the motor and sensory fibres. Spinal cord injuries at high cervical levels may cause paralysis of the diaphragm, resulting in ventilatory failure. Tumours within the spinal cord are called intrinsic , those outside the cord but compressing it are called extrinsic.

Intrinsic tumours include ependymomas and astrocytomas, which are malignant, and angiomas and cysts, which are benign. Cancer of the breast, lung, kidney, or prostate gland can cause extrinsic tumours of the spinal cord.

Facing cranial nerve assessment

Other tumours arising outside the cord include lymphomas, lipomas, neurofibromas, meningiomas, and chordomas. All of these can cause spinal nerve irritation, with pain and tingling, at the level of the tumour. Diagnosis of a tumour is confirmed by myelography , usually with computed tomography CT scanning or magnetic resonance imaging MRI. Raised protein levels or malignant cells in the cerebrospinal fluid may also confirm a tumour. Surgery and radiation therapy are the principal treatments. Subacute combined degeneration, which results from a vitamin B 12 deficiency, causes demyelination of the corticospinal and the dorsal columns.

Much of the damage is to the large dorsal-root ganglion neurons; the peripheral nerve fibres also demyelinate, so that peripheral neuropathy also occurs. Symptoms include tingling, numbness, weakness, mental disturbances, and vision changes. Treatment with vitamin B 12 may lead to improvement. Diseases of the blood vessels are uncommon in the spinal cord. When blockages of vessels do occur, causes include severe atherothrombotic disease of the aorta, aortic or thoracic surgery, bleeding from an arteriovenous malformation , or arterial compression by a tumour or prolapsed disk.

Neurological Assessment

Damage to the anterior three-quarters of the cord is common because this area is supplied by only the ventral spinal artery. The dorsal columns and the dorsal-root entry zone usually escape damage because they are supplied by three or more dorsal spinal arteries. Radiation therapy for certain cancers may cause a slow but progressive deterioration of the roots and tracts at the irradiated level of the cord. Myelopathy often leads to spastic weakness of the legs and to less obvious sensory changes.

Syringomyelia is frequently associated with obstructions of the roof foramina, or openings, of the fourth ventricle of the brain. Increased pressure of the cerebrospinal fluid enlarges the canal and ultimately causes a cavity, or syrinx, to branch out from the spinal canal and enlarge over years. As a result, sensory fibres, traveling from the dorsal-root entry zone to the opposite spinothalamic tract and to ventral-horn neurons at the same level, are interrupted. In addition, compression of the corticospinal tracts occurs.

Interruption of the dorsal-root—ventral-horn connection, which mediates reflex activity, results in loss of stretch reflexes and atrophy of some muscles innervated at that level. Interruption of the spinothalamic fibres, which transmit sensory impulses from both sides of the body to the thalamus, causes a loss of light touch, temperature, and pain sensations, as well as signs of an upper motor neuron lesion below the level of the cavity. Some perception, such as position sense, is retained. This is an example of dissociated sensory loss, which is also found in some brainstem lesions, transection of half of the spinal cord, and certain peripheral neuropathies.

Surgical drainage of the cavity, to prevent pressure from distending it further, may result in improvement. Demyelinating diseases frequently affect the spinal cord, particularly the corticospinal tracts and dorsal columns. The only features of Devic disease, a variant of multiple sclerosis, are a band of spinal cord inflammation and demyelination and optic nerve involvement.

Brief, involuntary jerks of the trunk and of the limbs may occur in spinal myoclonus. Many diffuse, metabolic, or local structural causes of myoclonus are possible, and the disease commonly originates in the brainstem or in the cerebral hemispheres. Damage to the olfactory nerve can occur from a head injury, local nasal disease, or pressure from a tumour and may result in reduced sensitivity to smell or a complete loss anosmia on the side supplied by the nerve.

Damage to the nerve may also result in a loss of flavour perception. Hallucinations of smell may occur in brain disorders such as epilepsy, with the presence of a tumour, or in depressive illnesses. Disorders of the optic nerve or of the pathways traveling to the occipital lobe cause visual loss in the affected eye. In the early stages of disease, when the optic process is irritating the nerve rather than decreasing its conducting ability, phenomena such as streaks of light may be seen.

When the optic pathways are affected within the brain, the precise location of the disease can be determined by testing the pattern of visual loss affecting both eyes. Pain in the eyes is sometimes due to neuritis of the optic nerves, but it is usually caused by ocular disease. Optic neuritis causes a total or partial loss of vision. It is a condition that is occasionally inherited, but it may also occur because of infection, drug or chemical toxicity, ischemia, or demyelinating disease.

Compression of the nerve by a tumour or aneurysm may eventually cause demyelination, which results in optic atrophy. Papilledema is a condition characterized by a swelling of the nerve head with fluid as a result of raised intracranial pressure.

Analyzing the role of diet and exercise in myelin production

Compression of the oculomotor, trochlear, or abducens nerves may be caused by lesions , diabetes, vascular disease, head injury, infection, or neuropathy. In the brainstem, multiple sclerosis , stroke , Wernicke disease see below Brainstem , and tumours are possible causes of compression. Double vision is the primary symptom; if the oculomotor nerve is affected, the pupil may be enlarged as well.

In Horner syndrome, interruption of the long sympathetic fibres passing from the brainstem to the pupil causes drooping of the eyelid and a small pupil. Argyll Robertson pupils, small and irregular pupils that do not react to light but constrict on accommodation to close vision, may be associated with syphilis or other brainstem diseases. Adie pupils constrict very slowly in light and dilate slowly when the light is removed.

In progressive external ophthalmoplegia, a disorder of the central nervous system mechanisms controlling gaze, the eyes may fail to move in one or another direction. Other neurological problems, such as parkinsonism, dementia, or neuropathy, may be associated with this condition. Local lesions of the brainstem may also cause paralysis of eye movement, as may severe myasthenia and myopathies affecting the eye muscles. The jerky eye movements of nystagmus usually signify brainstem, vestibular, or cerebellar disease, but they may also be complications of very poor eyesight or may occur as a congenital defect.

When any of the three oculomotor nerves are affected, the axes of the eyes are not able to remain parallel, so light falls on different parts of the two retinas and double vision results. Numbness of the face is commonly due to compression of the trigeminal nerve caused by a tumour in the cranial cavity or nasopharynx or by a brainstem disorder.

Trigeminal neuralgia , also called tic douloureux, is an intense, repetitive, pain felt in the lower half of one side of the face. It occurs primarily in people over 55 years of age. Symptoms may be relieved by medications such as carbamazepine, diphenylhydantoin, or baclofen or by surgical removal of a loop of normal artery where it impinges upon the nerve at its exit from the brainstem. The facial nerve is damaged most commonly by swelling within the facial canal in the temporal bone that results from viral infection.

This causes Bell palsy , an abrupt weakness of all the facial muscles on one side of the face that is often accompanied by pain around the ear, unusual loudness of sounds on the same side, and loss of taste on the front of the tongue. In hemifacial spasm repetitive twitching of one side of the face occurs. Irritation of the facial nerve as it leaves the brainstem appears to be the cause, and in many cases relief is obtained through surgical decompression.

When both divisions of the vestibulocochlear nerve are affected by disease, symptoms may include ringing in the ear tinnitus , a sensation of spinning vertigo , and other symptoms such as deafness. Deafness, if not caused by middle-ear disease, suggests damage to the cochlear portion of the nerve. Benign postural vertigo is characterized by brief severe attacks of vertigo induced by movement, especially turning in bed. The condition is less persistent than vestibular neuronitis, in which severe vertigo persists for days, probably as a result of viral infection of the inner ear or vestibular nerve.

In this context , the term bulbar refers to the medulla oblongata, which looks like a swelling, or bulb, at the top of the spinal cord. Damage to the 9th through 12th cranial nerves, the bulbar nerves, causes impairment of swallowing and speech and weakness of the neck muscles. These paralyses often lead to choking and asphyxia due to inhalation of saliva and food and inability to swallow or clear the airway of secretions that may be aspirated into the lungs. A nasal tone to the voice and weakness of coughing are early signs of damage to these nerves.

Causes of bulbar palsy include motor neuropathies, such as diphtheria , poliomyelitis , and botulism , motor neuron diseases, myasthenia gravis , certain muscle diseases, and compression of the nerves by tumours. Brainstem lesions produce a number of syndromes depending on their location and cause. In Moebius syndrome, the abducens and facial nerves, which originate in the brainstem, do not develop. Encephalitis may affect the brainstem only, with consequent damage to cranial nerves, to cerebellar connections, to the long ascending and descending tracts in the pons and medulla oblongata, and to the reticular activating system and short tracts within the brainstem that control the functions of consciousness and coordinate eye movements.

Strokes , malignant tumours such as gliomas, and multiple sclerosis also may affect this region. In syringobulbia a cavity forms within the brainstem in association with syringomyelia see above The spinal cord that causes cranial nerve palsies and both cerebellar and long-tract symptoms. Wernicke disease is caused by a thiamine vitamin B 1 deficiency and occurs most often in alcoholics; symptoms include ocular palsies, nystagmus, memory disturbance, and peripheral neuropathy.

Eye symptoms may be corrected by the administration of thiamine. Correction of severe sodium depletion may cause edema , or accumulation of fluid, in the central nervous system. Since many motor nerve fibres cross over and intertwine in the pons , the resulting swelling may lead to their compression and dysfunction, as well as to demyelination, a condition known as central pontine myelinolysis. Unconsciousness and spastic paralysis of the limbs are the primary symptoms. The raphe nuclei of the pons and the locus ceruleus, which mediate sleep , are situated in the brainstem.

During non-REM sleep an individual progresses from drowsiness through deeper and deeper levels of relaxation, with decreasing ability to be aroused; progressively slower waveforms appear on an electroencephalogram EEG during this phase. Periods of REM sleep, during which dreaming occurs, punctuate slow-wave sleep. Paradoxically, although the individual appears deeply asleep, fast activity occurs on an EEG during this phase, and numerous brief, small-amplitude movements are made by the eyes and the muscles.

Narcolepsy is a genetic disorder in which, with little warning, irresistible sleepiness overcomes a person during the day. One form includes vivid hallucinations on awaking or falling asleep, temporary but profound sleep paralysis on awakening that does not affect breathing, and sudden, brief loss of muscle power in the limbs and trunk during emotional moments such as laughter cataplexy. Increased sleepiness, or hypersomnia, may be the cause of drowsiness or narcolepsy. Narcolepsy may be described as an intrusion of REM sleep into the waking hours.

Treatment of the disorder with stimulants and tricyclic medications is often effective. Brain death is synonymous with brainstem death, since the control centres for essential functions such as consciousness, respiration, and blood pressure are located within the brainstem. In many countries strict criteria for diagnosis of brain death have been established by common consent among medical, religious, ethical , and legal experts. Signs of brain death include the presence of deep coma with an established cause and the absence of any brainstem functions, such as spontaneous respiration, pupillary reactions, eye movements, and gag and cough reflexes.

EEG may be a useful confirmatory test. When brainstem death is confirmed, the heart usually stops beating within a day or two, even when other vital functions are artificially maintained. Spinocerebellar degenerations are a group of inherited disorders characterized by atrophy of the central nervous system and of peripheral nerves. They commonly affect the cerebellum and its connections, as well as the nuclei in the medulla known as the olives, the centres for control of eye movements, the optic nerves, the dorsal columns of the spinal cord, and the corticospinal tracts.

Onset is usually in the first two decades of life. Some patients show only minimal signs, although most conditions are slowly progressive. Friedreich ataxia , the prototypical spinocerebellar degeneration disorder, affects the optic nerves, dorsal columns, corticospinal tracts, and cerebellum.

Peripheral neuropathy, skeletal deformities, high-arched feet, and rotation of the spine scoliosis also may occur. Inflammatory diseases affecting the cerebellum comprise abscesses, which usually complicate chronic infections of the middle ear through the spread of infection along the veins draining back into the posterior fossa, cerebellitis, associated with some viral infections in children, and tuberculomas, inflammatory masses that act as tumours, raising intracranial pressure and causing cerebellar dysfunction.

Cerebellar hemorrhage may occur with high blood pressure , causing sudden headache, neck stiffness, and cerebellar signs, often with evidence of compression of the brainstem on the side of the bleeding. Prompt surgical evacuation of the blood clot is necessary, and the availability of computed tomography CT scanning aids in diagnosis. Infarcts of the cerebellar arteries may also affect part of the medulla oblongata or pons. Demyelination frequently affects the cerebellum and its connections.

The primary signs of cerebellar disease are nystagmus, ataxia, and scanning speech. See Unlocalized or multifocal disorders: Demyelinating diseases. Chronic alcoholism, toxicity of diphenylhydantoin an antiepileptic medication , thiamine and nicotinic acid deficiencies, and hypothyroidism may all cause cerebellar dysfunction. In all of these disorders, typical signs of truncal and limb incoordination, or ataxia, are detectable; treatment usually reverses the deficits. Numerous inherited metabolic defects of metal, lipid, or amino acid metabolism see below Unlocalized or multifocal disorders and some serum protein abnormalities also cause signs of cerebellar disease.

Benign tumours, usually schwannomas on the vestibulocochlear nerve , may compress the cerebellum and lead to dysfunction on one side, but malignant astrocytomas and metastases from cancers are more common. In children, medulloblastomas are fast-growing malignant tumours that destroy the central part of the cerebellum and cause severe gait ataxia.

Astrocytomas grow much more slowly and can often be completely removed. Parkinson disease is a progressive disorder caused by degeneration of the cells of the substantia nigra and locus ceruleus both pigmented nuclei in the brainstem and of their connections with the basal ganglia. The basal ganglia are nuclear masses situated above the brainstem that are involved with the initiation and patterning of voluntary movements. This motor control system uses the neurotransmitters dopamine and acetylcholine ; in parkinsonism there is a deficiency of dopamine as a result of the degeneration of neurons in the substantia nigra.

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This leads to inhibition of activity within the basal ganglia. Most cases of parkinsonism occur in late middle age. Slowness of movement, muscle rigidity, stooped and flexed posture, and repetitive tremor of the limbs are the main symptoms of Parkinson disease. Depression and loss of intellectual agility are also common. The cause of Parkinson disease is unknown, although encephalitis in early life, many drugs and toxic chemicals, brain trauma, cerebral anoxia, and other degenerative diseases of the nervous system e.

The medication levodopa , or l -dopa, a precursor of dopamine that crosses the blood-brain barrier into the brain, where it encourages the synthesis of the deficient neurotransmitter, is the primary treatment. Other treatment approaches include anticholinergic medications, which reduce activity in the basal ganglia; medications such as bromocriptine and pergolide, which augment the responsiveness of the receptor sites where dopamine normally exerts its effect; amantidine, which increases dopamine release; and selective inhibitor medications such as deprenyl, which block the action of the enzyme that breaks down dopamine.

If treatment with medication is not successful, surgery may be performed to destroy the area of the brain that produces tremors. Dystonias, sustained muscular contractions that produce abnormal postures of the face, head, trunk, and limbs, are caused by disease of the basal ganglia. Other abnormal involuntary movements, such as vocalizations, tremors, and jerks, may also occur. Generalized dystonia e.

The intensity of the movements may be so severe that self-care is impossible. Although a number of medications are effective in reducing the movements, surgical destruction of the ventrolateral nucleus of the thalamus may be performed to relieve muscle rigidity in severe cases. Tics are similar to dystonia, but they consist of brief movements or utterances of unknown cause. In severe cases, sudden, explosive speech or movements occur repeatedly, as in people with Tourette syndrome.

Chorea is characterized by brief and involuntary dancelike movements that are usually seen with disease of the caudate nuclei, which are part of the basal ganglia. Huntington disease is an inherited form of chorea that leads to dementia and early death but is usually asymptomatic until adulthood.

Presymptomatic diagnosis can be determined by genetic testing. Early symptoms of the disease include personality changes, such as irritability and depression, and an inclination to alcohol abuse. This is followed by intellectual deterioration with paranoia and brief, jerky movements of the limbs and face or, less commonly, muscle rigidity. Medications such as phenothiazine or butyrophenone may reduce the movements.

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They may use inappropriate words, which do not make sense to the assessor, or they may make incomprehensible sounds such as moans or groans. Some stimuli may be required to obtain a response from the patient - this type of patient is not aware of their surroundings. When a patient does not respond to simple commands then response to painful stimuli is assessed. There are three recognised stimuli that can be used when assessing motor response:. The advantage of the GCS is that it is widely known and used and provides a standardised assessment of neurological observations.

It is simple to use and requires only a pen torch with a bright beam and a copy of the assessment tool. However, Ellis and Cavanagh cited in Woodrow, have noted that there may be variations in the recording of pupil size and motor weakness. Nurses therefore need to be educated in the correct use of the tool, in order to address potential irregularities.

There is no published consensus on how frequently neurological observations should be recorded. For example, the patient may have a known neurological disease such as multiple sclerosis, or may have had a previous cerebral vascular accident, both of which could affect the outcome of the assessment. Nurses need appropriate training in order to achieve accurate assessment. The GCS is widely used in the management of patients with actual or potential neurological problems. Neurorehabilitation service prover, the Christchurch Group, has appointed Sue Houston, as its new head of nursing.

New best practice training guidelines have been published for professional carers administering buccal ormomucosal midazolam for epilepsy patients in the community. Miss any of the news affecting the profession during March ? Catch up with our summary of the main nursing headlines. Older people living in nursing homes and who take part in a regular, organised exercise programme gain multiple benefits, including a reduced falls risk and less frailty, according to Spanish researchers.

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Menu Home News Back. Your browser is no longer supported For the best possible experience using our website we recommend you upgrade to a newer version or another browser. Learn more Agree. Sign in. Search the site Search. CLINICAL FOCUS Getting patients up and moving shortens length of hospital stay A meta-analysis of 13 studies shows that encouraging medical inpatients to get out of bed and mobilise improves their walking ability and reduces their length of stay in hospital.

Student Blogs: 'A clinical academic PhD helped me to develop myself through learning' 2 July, am 'A practice placement is your opportunity to shine' 26 June, pm 'As a society we need to reshape our perception of nursing' 21 June, am 'I hope my story will inspire others to consider a career in caring for children' 19 June, am More blogs from student nurses. On the pulse Closing facilities with unsafe staffing may send a message politicians understand It seems to me that, these days, we hear more and more about wards or even hospitals closing because of nursing staff shortages.

Your Nursing Career Attend a careers fair Career inspiration. Student subscription This subscription package is aimed at student nurses, offering advice and insight about how to handle every aspect of their training. You are here: Neurology. Neurological observations. Levels of consciousness Consciousness can be categorised as:.