COMMON NEUROLOGICAL HEALTH PROBLEMS NCM 104

Neural Tube Defects Risk Factors: Maternal malnutrition Drug exposure Low socioeconomic group Older maternal age Genetic predisposition Types: Anencephaly Spina Bifida occulta Meningocele Myelomeningocele Encephalocele Anencephaly Upper end of the neural tube-Fails to close in early intrauterine lifeAbsence of the cerebral hemispheres Clinical Manifestations Elevated level of alpha-fetoprotein in maternal serum/or amniocentesis May survive for a number of days after birth Spina Bifida Occulta Description Occurs when the posterior laminae of the vertibrae fail to fuse Occurs most commonly in the 5th lumbar or 1st sacral level Clinical Manifestations Most patient have no symptoms Dimple in the skin or growth of hair over the malformed vertebra There is no externally visible sac Syringomyelia Tethered cord With growth the child may develop: Foot weakness Bowel and bladder sphincter disturbances Meningocele Description : CSF and covered with skin Clinical Manifestations External cystic defect in the midline of spinal cord Seldom evidence of weakness of the legs or lack of sphincter control Myelomeningocele The spinal cord and and meninges protrude through the vertebrae

Clinical Manifestations Flaccidity and lack of sensation of the lower extremities Loss of bowel and bladder control Lax legs Other symptoms TALIPES disorders or developmental HIP DYSPLASIA Arnold –Chiari malformation-Malformation of the brainstem and cerebellumBlock in the flow of CSFHYDROCEPHALUS Encephalocele A cranial meningocele or myelomeningocle Occurs most often in the occipital area of the skull Clinical Manifestations Build up of too much fluid in the brain Complete loss of strength in the arms and legs An unusually small head Uncoordinated movement of the voluntary muscles Developmental delay Visual problems Mental and growth retardation Seizures Diagnostic Evaluation Sonography Fetoscopy CT scan MRI Amniocentesis – inc. AFP Management Surgical correction-CAN BE DONE SOON AFTER BIRTH Laminectomy Closure of the open lesion Removal of the sac Purpose To prevent further deterioration of neural function To minimize the danger of rupture and infection To improve cosmetic effect To facilitate handling of the infant Ventriculoperitoneal shunt Nursing Management: Evaluate sac and measure lesion Perform neurological assessment Monitor increase in ICP Protect sac, use aseptic technique Protect skin integrity Place in prone position, head turned to one side for feeding Assess for early signs of infection Administer medication as ordered Cerebral Palsy

postmaturity Birth asphyxia Early infection or trauma Maternal anemia Genetic Factors Clinical Manifestations Tones remains relatively constant regardless of activity and level of arousal Significant Hyperreflexia Stiff and rigid arms or legs Extreme irritability and crying Feeding difficulties Delayed gross development Opisthotonus posture Management Antispasticity medications Dantrolene (Dantrium) Diazepam ( Valium) Botulinum Toxin A: Botox Therapies: speech.Description: A group of nonprogressive dysfunction Risk Factors: UNKNOWN Associated with Complications of birth. physical.Prematurity. occupational Botulinum Toxin A: Botox Massage Prosthetics/Orthotics Surgery .

appropriate toys for age and developmental level Position upright after meals Reye’s Syndrome Description: Acute encephalitis with accompanying fatty infiltration of the liver. nausea & vomiting. stupor. Seizures Respiratory arrest Hypothrombinemia Hypoglycemia Elevated blood ammonia levels Elevated liver enzyme Treatment No specific treatment exists No cure: Recovery is dependant on severity of brain swelling Faster progression worse prognosis Nursing Management Frequent neurologic assessment Supporting respiratory function Controlling hypoglycemia Reducing brain edema MULTIPLE SCLEROSIS ( MS) Description A chronic demyelinating disease that affects the the myelin sheath of neurons in the central nervous system Characterized by periods of REMISSION and EXACERBATION Usually occurs between 20 to 40 years of age Affect women twice as often as men Race -Whites Most prevalent in colder climates of North America and Europe CAUSES . lethargy. lungs. deep coma. pancreas. heart. neurologic impairment Anorexia Agitation Confusion Combativeness Confusion . and skeletal muscles Risk Factors Generally unknown Occurs after varicella. influenza if the child is treated with aspirin Clinical Manifestations Lethargy. not on chronological age level Provide safe environment Provide safe.Hyperbaric Oxygen Nursing Management Assess child’s developmental level and intelligence Encourage early intervention and participation in school programs Prepare for using mobilizing devices to prevent deformities Communicate with the child on a functional level.

Unknown Genetic susceptibility Autoimmune ( post viral infection) Epstein –Barr virus PRECIPITATING FACTORS Infection Physical injury Emotional stress Pregnancy Fatigue Clinical Manifestations CHARCOT’S TRIAD Scanning speech( dysarthia) Intentional tremors Nystagmus Visual Disturbances Blurring of vision Diplopia Patchy blindness Total blindness Sensory Nerve Disturbances Peresthesia Proprioception loss Pain Cognitive Disturbances Memory loss Decreased concentration Dementia .

standard therapy for acute exacerbation Muscle Relaxants Baclofen ( medication of choice for spasticity ) Antiepileptic Drugs Anti depressants Stimulant Drugs Cholinergic Anti cholinergic Nursing Management Promoting physical mobility Walking Use of assistive devices Others Warm packs Avoid hot baths Avoid strenuous exercises MYASTHENIA GRAVIS Description : Chronic autoimmune disorder affecting the neuromascular transmission of impulses in the voluntary muscles of the body Causes Unknown Autoimmune Women are 3X more susceptible Clinical Manifestations Extreme muscle weakness and fatigue Diplopia & Ptosis Dysarthia Generalized weakness Respiratory paralysis .Poor abstract reasoning Cerebellum/ Basal Ganglia Involvement Ataxia Tremors Weakness of muscle in throat and face OTHERS: Bowel and Bladder dysfunction Impotence Muscle hypertonicity Medical Management: Immunomodulating Drugs Interferon beta -1b (Betaseron ) Interferon beta-1a (Rebif) Immunosuppresant Drugs Azathioprine Cyclophosphamide Corticosteroid Drugs Methylprednisolone.

Diagnostic Tests Serum test for acetylcholine receptor antibodies Edrophonium (Tensilon) test IV injection relieves symptom temporarily After injection a marked but temporary improvement in muscle strength suggest MG CT scan EMG Decremental response to repetitive nerve stimulation Treatment Anti cholinesterase Pyridostigmine ( Mestinon) Neostigmine( prostigmin) Immunosuppressive therapy Prednisone Imuran (azathioprine) Plasmapheresis Thymectomy TREATMENT Plasmapheresis Removes the antibodies which cause weakness Benefits in 70% of patients within two weeks Few serious side effects More difficult to arrange short notice Thymectomy Surgical removal of the thymus It can produce antigen-specific immunosopression The patient benefit from the procedure after 3 years and above because of the long life circulating T cells .

400 times more common in patients with MS Common to 50 to 70 years old Causes Unknown Degenerative Chronic compression or irritation of trigeminal nerve Degenerative changes Viral causes suspected Compression from artery adjacent to the nerve strips myelin from nerve when it pulsates .Medications to be AVOIDED Muscle relaxant Barbiturates Morphine sulfate Tranquilizers Nursing Interventions Assess gag reflex before feeding Place client in fowlers’ position Offer thick fluids Flex the neck during feeding Administer medication 20-30 minutes before meals Protect from falls due to weakness Start meal with cold beverages Avoid exposure to infection Provide adequate rest and activity Trigeminal Neuralgia AKA: Tic Douloureux DESCRIPTION: An intensely painful neurologic condition that affects one or more branches of the fifth cranial( trigeminal ) nerve.

May equally happened to both sexes Occurs most commonly between ages 20 and 40 years Causes Unknown Autoimmune Viral Bacterial infection .Clinical Manifestations Intense recurring episodes of pain Episodes of pain begin and end suddenly Unilateral pain Numbness particularly around corner of the mouth Diagnostic Test History of symptoms and direct observation of an attack CT scan MRI Medical Management Pharmacologic Therapy Carbamezepine ( Tegretol ) Imipramine ( Tofranil) Phenytoin ( Dilantin) Gabapentin ( Neurontin) Alcohol or phenol block injection Surgical Treatment Radiofrequency Thermal Coagulation Microvascular Decompression of the trigeminal Nerve .Removing the vessel from the posterior trigeminal nerve Rhizotomy Nursing Management Recognize factors that may aggravate facial pain Providing cotton pads and temperature water for washing the face Rinse with mouthwash after eating Chew on the unaffected side Soft foods Postoperative care Sensory deficits Instruct not to rub the eye Assess the eye for irritation or redness Artificial tears Bell’s Palsy Description : Acute peripheral facial paralysis of the infratemporal portion of the seventh cranial( Facial ) nerve unilaterally.

Clinical Manifestations Inability to close eye completely on the affected side Ptosis Pain around the jaw or ear Unilateral facial weakness Ringing in the ear Eating difficulty Flat nasolabial fold Photophobia Diminished taste from anterior two thirds of the tongue Decreased lacrimation Diagnostic Tests History and Physical Exam EMG Management Medications Prednisone Analgesics Antiviral drugs Comfort measures Heat application Gentle massage Electrical nerve stimulation Nutrition: Soft diet Instruct to chew on the unaffected side Avoid hot fluids /food Administer medications as ordered Artificial tears is recommended .

sensory or visual function TIA’s should not be ignored!!!!! More that 1/3 of people will go on to have an actual stroke 5% of strokes will occur within 1 month of the TIA or first stroke 12% will occur within 1 year 20% will occur within 2 years 25% will occur within 3 years 2. Transient ischemic attack ( TIA) CAUSES: Atherosclerotic plaque or thrombosis. inc. po2.Eye patch at night Facial exercise CEREBROVASCULAR DISEASE 1. dec. Pco2. dec.Cerebrovascular Accident Description: The rapid loss of brain function due to disturbance in the blood supply to the brain. Onset and persistence neurologic dysfunction lasting longer than 24 hours Indicates infarction rather than ischemia Risk Factors Hypertension Heart disease .Cerebrovascular Insufficiency Description An interruption or inadequate blood flow to a focal area of the brain resulting in transient or permanent neurologic dysfunction. blood viscosity Transient Ischemic Attack Description : Neurologic deficit typically lasting less than 1 hour sudden loss of motor .

occurs rapidly Numbness or weakness of the face. permanent loss of function with SLOWER. dizziness. LESS COMPLETE recovery Rapid progression into COMA Medical Management Thrombolytic Therapy Recombinant tissue plasminogen activator (rt-PA) 0. or leg. or loss of balance or coordination Sudden. arm. patients need to get to the hospital within 60 minutes.9 mg/kg TIV over 1 hour TIME IS BRAIN Time is very important in order to receive this medication Window of opportunity to start treating stroke patients is three hours. especially on one side of the body Confusion or change in mental status Trouble speaking or understanding speech Visual disturbances Difficulty walking. severe headache with no known cause Hemorrhagic Stroke Clinical Manifestations Severe headache and nuchal rigidity Rapid onset of complete hemiplegia occurs over minute to 1 hour Usually results in extensive .Elevated cholesterol DM Cigarette smoking TIA Obesity Carotid stenosis Polycythemia DIAGNOSTIC EVALUATION CT scan or CAT scan ECG Carotid ultrasound Cerebral angiography PET MRI ISCHEMIC STROKE Clinical Manifestations Thrombosis -Tends to develop during sleep or within 1 hour of arising Embolism – No discernible time pattern. but to be evaluated and receive treatment. Platelet-inhibiting medications Analgesics Antihypertensive medications Antihyperlipidemic drugs Surgical Management Surgical Evacuation (Craniotomy) if Cerebellar hemorrhage diameter exceeds 3 cm . unrelated to activity .

Riluzole Other Drugs: Baclofen (Lioresal). Pupil size Provide safety measures ( Hemianopsia) Manage Dysphagia Manage Motor deficits Manage verbal deficits Manage cognitive deficits Amyotrophic Lateral Sclerosis Other term: Lou Gehrig’s Disease Description: A progressive . Dantrolene sodium (Dantrium). or . degenerative condition that affects motors neurons responsible for control the control of voluntary muscles Causes unknown. restful environment Position Lateral ( initially).Glasgow Coma Scale score is below 14 Aneurysm Clipping Craniectomy Carotid Endarterectomy Carotid stenting NURSING MANAGEMENT Prevent shoulder adduction Ensure patent airway Give 100% O2 Maintain a quiet. Low fowlers with neck aligned( stable) Minitor VS. GCS. Autoimmune Free radical damage 5-10% genetically transmitted Over –excitation of the neurotransmitter GLUTAMATE Clinical Manifestations Fatigue Muscle weakness Cramps Fasciculation Dysphagia DOB Inappropriate emotional outburst of laughing and crying Constipation Urinary urgency problem Diagnostic Tests Electromyography Muscle biopsy MRI EEG CSF Medical Management Glutamate Antagonist .

emotional & physical abilities History of progressive memory loss & regressive behavior Physical & emotional status in relation to needs associated with nutrition. IRREVERSIBLE . DEGENERATIVE. & safety History of premorbid personality from family members History of medications used by client Clinical Manifestations WARNING SIGNS Memory loss affecting ability to function in job Difficulty with familiar tasks Problems with language and abstract thinking Disorietation. changes in mood and personality . Mechanical ventilation (using negative-pressure ventilators) Nursing Management Maximize Functional abilities Ensure adequate nutrition Prevent respiratory complications Help client and family deal with current problem Alzheimer’s Disease Description : PROGRESSIVE .Diazepam (Valium) Enteral feeding. Autoimmune Viral/ Bacterial Infection Trisomy 21 ( 40 y/o) Decrease in the level of acetylcholine transferase activity in the cortex and hippocampus Assessment findings History of progressive degeneration of mental. neurologic disease Begins with gradual losses of cognitive function and disturbances in behavior and affect Causes Unknown. fluid & electrolyte status.

small frequent feeding Encephalitis Clinical Manifestations Headache & fever Nuchal rigidity Confusion Decreased level of consciousness Seizures Sensitivity to light . emotional and social aspect Medication regimen Safety measures Signs and symptoms of disease progression CNS INFECTION /INFLAMMATORY DISTURBANCES Meningitis Description An inflammation of the lining around the brain and spinal cord Causes : Bacterial (Neisseria meningitidis ) Viral Fungal (cryptococcus) Clinical Manifestations Headache and Fever Positive kernig’s signs Positive Brudzinki’s sign Photophobia Nuchal rigidity Opisthotonus Diagnostic Test Bacterial culture and gram staining of CSF and blood through lumbar puncture Medical Management Vancomycin Cephalosporins Dexamethasone Fluid volume expanders Nursing Management Administer large doses of antibiotics IV as ordered Respiratory isolation for 24 hours after initiation of antibiotic therapy Analgesic as ordered Maintain F & E balance Provide emotional support for patients Decrease stimuli from the environment Position on the side with head gently supported in extension Monitor daily body weight Diet : high calorie.Nursing Management Health teaching Address physical. high protein.

usually worse in the morning Vomiting Weakness of an extremity Decreasing vision Seizures Change in mental status Fever may or may not be present Diagnostic Test Computed tomography (CT) scan Magnetic resonance imaging (MRI) . ears. Causes Intracranial trauma or surgery Sinuses.Ataxia Abnormal sleep patterns Tremors Hemiparesis Diagnostic Tests CT scan MRI Lumbar Puncture EEG Medical Management Anticonvulsants Antipyretics Analgesics Sedatives Antiviral ( Acyclovir) Nursing Management Monitor VS Perform neurological assessment Comfort measure to reduce headache Injury prevention Brain abscess Description It is a complication encountered increasingly in patients whose immune systems have been suppressed either through therapy or disease. and teeth Otitis media Dental sepsis Spread of infection from other organs Clinical Manifestations Headache.

Medical Management Penicillin G and Chloramphenicol Corticosteroids Phenytoin Phenobarbital CT-guided stereotactic needle aspiration under local anesthesia Nursing Management Monitor V/S Perform neurological assessment frequently Administer medications as ordered Assess client response to treatment Providing supportive care Monitor blood glucose and serum potassium level Guillain.Barre syndrome Description Also called acute demyelinating polyneuropathy An autoimmune attack of the peripheral nerve myelin Acute .rapid segmental demyelination of peripheral nerves and some cranial nerves More frequent in males Causes Unknown Autoimmune ( post viral infection) Diagnostic Tests EMG CSF ECG Clinical Manifestations Diminished reflexes and muscle weakness that goes upward .

related injuries .Clumsiness Paralysis of the diaphragm Dysphagia Respiratory depression Paresthesia Paralysis of the ocular muscles Ataxia Complications Respiratory failure Cardiac dysrhythmia Transient hypertension Orthosthatic hypotension Pulmonary embolism Medical Management IV immunoglobulin Plasmapheresis Cortecosteroids Nursing Management Mostly supportive Maintain adequate ventilation Incentive spirometry CPT Perform ROM Assess gag reflex Monitor VS Administer corticosteroids Trauma ( Cranio –cerebral-and spinal) Head Injury Description : Also known as traumatic brain injury( TBI) The disruption of normal brain function due to traumatic related injury resulting in neurologic functions Causes : Blunt or penetrating injury Motor.vehicle accidents are the leading cause of head injuries Falls and sports.

with possible surface hemorrhage. corpus callosum.Types of Brain injuries Concussion a temporary loss of neurologic function with no apparent structural damage. Brain stem contusion Cerebral contusion Diffuse axonal Injury Widespread damage to axons in the Cerebral hemispheres.Vertigo Agitation . ICP Establish an IV line of PNSS or PLR. Surgery for : Evacuation of intracranial hematomas Debridement of penetrating wounds Elevation of skull fracture Repair of CSF leaks Pharmacologic interventions Diazepam (Valium) Steroids Mannitol (Osmitrol) Barbiturate Antibiotics Nursing Management Emergency Care . Intracranial Hemorrhage Epidural hematoma or hemorrhage Subdural hematoma Intracerebral hemorrhage and hematoma Clinical Manifestations Altered level of consciousness: Confusion to coma Pupillary abnormalities Altered or absent gag reflex Absent corneal reflex Sudden onset of neurologic deficits Vision and hearing impairment Sensory dysfunction Spasticity Headache. and brain stem. restlessness Seizures Diagnostic Evaluation CT scan Skull and cervical spine films Glasgow Coma –Scale EEG Medical Management Management of inc. Contusion More severe injury in which the brain is bruised.fluid volume should be restricted.

Rhinorrhea Observe for S & Sx of inc. Incomplete cord damage prioception Partial loss of movement and sensation Bowel and bladder function Injuries to T1 and above Spinal and autonomic reflexes Paraplegia Intense and painful muscular spasms Injuries to T2 and below Autonomic Dysreflexia Tetraplegia Neurologic Level of injury Normal sensation and movement .base Record I and O balance Spinal Cord Injury Description A traumatic injury to the spinal cord Can range in severity from mild flexion. pressure. ICP .extension “ Whiplash” injuries to complete transection of the cord with permanent tetraplegia Etiology and Risk Factors Automobile or motorcycle accidents Gunshot or knife wounds Falls and sports mishaps Violence Most Common site of Injury C1-2 C4-6 T11-L2 CLINICAL MANIFESTATIONS Complete transection Below the level of injury. and undisturbed General Care Establish airway Prevent infection Prevent aspiration pneumonia Observe for CSF leakage Check for cardiovascular complications . temperature.Ensure a clear airway Keep spine straight Flexion or hyperextension should be avoided in case there is cervical fracture Keep patient covered. Lost of: All loss of function below the level of the Voluntary movement lesion Sensation of pain. quiet.Otorrhea Observe the skull and scalp injuries .Battle’s sign Control restlessness and pain Maintain adequate Nutrition Maintain F & E /electrolyte acid.

pressure. temperature. and vibration Contralateral loss of pain and temperature. usually of the cervical area Anterior Cord Syndrome Characteristics: Loss of pain. and motor function below the level of the lesion Light touch. position. Cause: Transverse hemisection of the cord (half of the cord is transected from north to south). usually as a result of a knife or missile injury Fracture dislocation of a unilateral articular process Possibly an acute ruptured disk. . and vibration sensation remain intact. Cause: acute disk herniation hyperflexion injuries associated with fracture-dislocation of vertebra. Cause: Injury or edema of the central cord.EFFECTS OF SPINAL CORD INJURY Central Cord Syndrome Characteristics: Motor deficits (in the upper extremities compared to the lower extremities Sensory loss varies but is more pronounced in the upper extremities Bowel/bladder dysfunction is variable. injury to the anterior spinal artery Brown-Sequard Syndrome (Lateral Cord Syndrome) Characteristics: Ipsilateral paralysis or paresis loss of touch. or function may be completely preserved.

complication – 12 weeks Management of complications Rehabilitation BRAIN TUMOR Description A localized intracranial lesion that occupies space within the skull. sandbags.Management Immediately after trauma ( Less than 1 hour ) Immobilization with rigid cervical collar.8 weeks Complete motor injury. and rigid spine board Methylprednisolone IV given within 8 hours of injury Acute Phase ( 1 to 24 hours ) Maintenance of pulmonary and cardiovascular stability Spinal cord immobilization Management of neurogenic bladder Pressure ulcer preventation Subacute Phase ( within 1 week) Traction and surgical interevntion GM -1 ganglioside sodium salt IV H2 receptor blockers Early mobilization and passive exercise Hyperalimentation Small doses of heparin Possible vena cava filter Neurogenic bowel program Chronic Phase ( Beyond 1 week) Anticoagulants Uncomplicated motor injury . Etiology Unknown Familial tendencies Immunosuppression Environmental factors .

Alterations in cognition Language disturbances ( aphasia ) .CLINICAL MANIFESTATIONS Headache Nausea and vomiting Papilledema Hemiparesis Seizures Mental status changes Sensory and motor abnormalities Visual alterations.

May last for 2 to 15 minutes autonomic Lasts for less than 1 minute . Partial Seizures Seizures beginning locally Repetitive purposeless beheviors Patient appears to be in a dream.Diagnostic Tests MRI CT Scan EEG Radionuclide scans Angiogram Lumbar puncture Stereotactic biopsy Pet scan Medical Management Chemotherapy Radiation therapy Brachytherapy Intravenous (IV) autologous bone marrow transplantation Surgery Craniotomy Laser resection or ultrasonic aspiration NURSING MANAGEMENT COMPENSATING FOR SELF-CARE DEFICITS IMPROVING NUTRITION RELIEVING ANXIETY ENHANCING FAMILY PROCESSES Seizure disorder Seizures Sudden abnormal and excessive electrical discharges from the brain that can change motor or autonomic function. chewing or smacking his or her lips 2.like state while picking at his/ her clothing. consciousness or sensation Epilepsy Chronic neurological disorder characterized by recurrent seizure activity Status Epilipticus One of a series of grand mal seizures lasting more than 30 minutes without waking intervals ETIOLOGIC FACTORS Idiopathic Drugs Traumatic brain injury Chemical poison Infection Drug and alcohol withdrawal Vascular diseases Allergies Classification 1. sensory.Generalized seizures Entire cerebral cortex is involved Types of partial seizures Simple Partial Complex Partial Does not loss consciousness Also termed as psychomotor seizure Symptoms confined to one hemisphere Consciousness is lost Affectation of the motor .

CT scan .Types of Generalized Seizures Absence Seizures Also referred to as Petit mal seizure Most often seen in children Manifested by a period of staring for several seconds Precipitated by stress. mild leukopenia Levetiracetam (Keppra) Somnolence. fatigue. dysrhythmias. irritability. fixed and dilated pupils. dizziness. nystagmus Nursing Management DURING SEIZURE Remove harmful object Ease the client to the floor Protect the head of the patient Observe the client thoroughly Loosen constrictive clothing Do not restrain or attempt to place tongue blade or insert oral airway AFTER SEIZURE Documents the event during and after the seizure Side –lying position Suction equipment should be available Place bed in low position Also termed as grand mal seizures Last for 30 to 60 seconds Characterized by rigidity. Cartagena RN. hypoglycemia. nausea and vomiting. hyperventilation Diagnostic Tests EEG . MAN Lecturer . unsteadiness. gingival hyperplasia. ataxia Phenytoin (Dilantin) Visual problems. diplopia. drowsiness. diplopia.dysarthria. hirsutism. fatigue Phenobarbital (Luminal) Sedation. hands and jaws are clenched Patient breathing may temporarily stop Urinary incontinence Cyclonic Repeated shock like. MRI Medical Management Common Anti-seizure Medication & their dose related S/E Carbamazepine (Tegretol) Dizziness. often violent contractions in one or more muscles Prepared by : Judith J.

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