DEMYELINATING DISEASES Jimmellee Ellen P.

Olilang, RN

 commonly called Lou Gehrig s disease  the most common of the motor neuron diseases causing muscular atrophy  onset occurs between ages 40 and 70; a chronic, progressively debilitating disease and is rapidly fatal affecting more men than women  the exact cause is unknown but 5% to 10% of the cases have a genetic component  it may result from: a slow acting virus nutritional deficiency related to a disturbance in enzyme metabolism autoimmune disorders that affect immune complexes in the renal glomerulus and basement membrane  there s loss of the nerve cell that control the muscles known as motor neurons.

CLINICAL MANIFESTATIONS: Loss of Motor neurons in the anterior 1. Fasciculations (involuntary twitching Horns of the spinal column or contraction of muscles) 2. Atrophy & weakness of in the muscles Motor nuclei of the lower brain of the forearms and hands stem die 3. Impaired speech Muscle fibers atrophies 4. Difficulty chewing and swallowing 5. Difficulty breathing Upper motor Neuron system Lower motor Neuron system 6. Choking 7. Excessive drooling 8. depression 9. Inappropriate laughing & crying spells

1. Aims to control symptoms & provide emotional,psychological & physical 2. Muscle biopsy support 3. CSF analysis reveals increase CHON 2. Patients who experience difficulty content swallowing may require nasogastric feedings TREATMENT: 1. Riluzole a neuroprotector to slow 3. Tracheotomy & mechanical ventilation deterioration of motor neurons in May be an option when hypoventilation develops the early stages 2. Baclofen, dantrolene sodium or diazepam may be given to control spasticity 3. Quinine therapy for painful muscle cramps

DIAGNOSTIC STUDIES: 1. Electromyography

NURSING CARE:

CLINICAL MANIFESTATIONS: Loss of Motor neurons in the anterior 1. Fasciculations (involuntary twitching Horns of the spinal column or contraction of muscles) 2. Atrophy & weakness of in the muscles Motor nuclei of the lower brain of the forearms and hands stem die 3. Impaired speech Muscle fibers atrophies 4. Difficulty chewing and swallowing 5. Difficulty breathing Upper motor Neuron system Lower motor Neuron system 6. Choking 7. Excessive drooling 8. depression 9. Inappropriate laughing & crying spells

MULTIPLE SCLEROSIS


An auto-immune mediated progressive demyelinating disease of the CNS The myelin sheath is destroyed and replaced by sclerotic tissue (sclerosis)

MULTIPLE SCLEROSIS
 

CAUSE- unknown Multiple factors- viral infection, environmental factors,geographic location and genetic predisposition Common in WOMEN ages 20-40

MULTIPLE SCLEROSIS
PATHOPHYSIOLOGY  Sensitized T cells will enter the brain and promote antibody production that damages the myelin sheath  Plaques of sclerotic tissues appear on the demyelinated axons interrupting the neuronal transmission

MULTIPLE SCLEROSIS
PATHOPHYSIOLOGY  The most common areas affected are
   

Optic nerves and chiasm Cerebrum Cerebellum Spinal cord

MULTIPLE SCLEROSIS
CLINICAL MANIFESTATIONS  1. visual problems such as diplopia, blurred vision and nystagmus  2. motor dysfunction  3. Fatigue  4. Mental changes like mood swings, depression  5. spasticity

MULTIPLE SCLEROSIS
  

DIAGNOSTIC TESTS 1. MRI- primary diagnostic study 2. CSF Immunoglobulin G

MULTIPLE SCLEROSIS
NURSING INTERVENTIONS 1. Promote physical mobility  Exercise  Schedule activity and rest periods  Warm packs over the spastic area  Swimming and cycling are very useful

MULTIPLE SCLEROSIS
NURSING INTERVENTIONS 2. Prevent injuries  Wide stance walking  Use of walking aids  Wheelchair

MULTIPLE SCLEROSIS
3. Enhance bladder and bowel control  Set a voiding schedule  Intermittent bladder catheterization  Use of condom catheter  Adequate fluids, dietary fibers and bowel training program

MULTIPLE SCLEROSIS
4. Manage speech and swallowing difficulties  Careful feeding, proper positioning, suction machine availability  Speech therapist

MULTIPLE SCLEROSIS
5. Improve Sensory and Cognitive function  Vision- use eye patch for diplopia  Obtain large printed reading materials  Offer emotional support  Involve the family in the care

MULTIPLE SCLEROSIS
6. Strengthen coping mechanism  Alleviate the stress  Referral to the appropriate agencies

MULTIPLE SCLEROSIS
7. improve self-care abilities  Modify activities according to physical strength  Provide assistive devices

MULTIPLE SCLEROSIS
8. promote sexual functioning  Refer to sexual counselor

MULTIPLE SCLEROSIS
MEDICAL MANAGEMENT Pharmacotherapy
    

Interferons Immunomodulators Corticosteroids BACLOFEN for muscle spasms NSAIDS for pain

Guillian-Barre Syndrome


An auto-immune attack of the peripheral nerve myelin Acute, rapid segmental demyelination of peripheral nerves and some cranial nerves

Guillian-Barre Syndrome


CAUSE: post-infectious polyneuritis of unknown origin commonly follows viral infection

Guillian-Barre Syndrome


PATHOPHYSIOLOGY


Cell-mediated imune attack to the myelin sheath of the peripheral nerves Infectious agent may elicit antibody production that can also destroy the myelin sheath

Guillian-Barre Syndrome
CLINICAL MANIFESTATIONS  1. Ascending weakness and paralysis  2. diminished reflexes of the lower extremities  3. paresthesia  4. potential respiratory failure

Guillian-Barre Syndrome
NURSING INTERVENTIONS 1. Maintain respiratory function  Chest physiotherapy and incentive spirometry  Mechanical vetnilator

Guillian-Barre Syndrome
NURSING INTERVENTIONS  2. Enhance physical mobility
   

Support paralyzed extremities Provide passive range of motion exercise Prevent DVT and pulmonary embolism Padding over bony prominences

Guillian-Barre Syndrome
NURSING INTERVENTIONS  3. Provide adequate nutrition
  

IVF Parenteral nutrition Assess frequently return o gag refelx

Guillian-Barre Syndrome
NURSING INTERVENTIONS  4. Improve communication


Use other means of communication

Guillian-Barre Syndrome
NURSING INTERVENTIONS  5. Decrease fear and anxiety
  

Provide Referrals Answer questions Provide diversional activities DVT, Urinary retention, pulmonary embolism, respiratory failure

6. Monitor and manage complications



Guillian-Barre Syndrome
MEDICAL MANAGEMENT  ICU admission  Mechanical Ventilation  TPN and IVF  PLASMAPHERESIS  IV IMMUNOGLOBULIN

ALZHEIMER S disease


A progressive neurologic disorder that affects the brain resulting in cognitive impairments

ALZHEIMER S disease
CAUSES:  Unknown  Potential factors- Amyloid plaques in the brain, Oxidative stress, neurochemical deficiencies

ALZHEIMER S disease
     

CLINCAL MANIFESTATIONS 1. Forgetfulness 2. Recent memory loss 3. Difficulty learning 4. Deterioration in personal hygiene 5. Inability to concentrate

ALZHEIMER S disease
   

 

LATE CLINICAL MANIFESTATIONS 6. Difficulty in abstract thinking 7. Difficulty communicating 8. Severe deterioration in memory, language and motor function 9. repetitive action- perseveration 10. personality changes

ALZHEIMER S disease
DIAGNOSTIC TEST  Neurologic examinat  EEG, CT and MRI  Other tests to rule out Vit B deficiencies and hypothyroidism  Autopsy is the most definitive

ALZHEIMER S disease
Drug therapy  1. drugs to treat behavioral symptoms- antipsychotics  2. anxiolytics  3. Donepezil  4. Tacrine

ALZHEIMER S disease
Nursing Interventions  1. Support patient s abilities  2. Provide emotional support

ALZHEIMER S disease
Nursing Interventions 3. Establish an effective communication system with the patient and family  Use short simple sentences, words and gestures  Maintain a calm and consistent approach  Attempt to analyze behavior for meaning

ALZHEIMER S disease
4. protect the patient from injury  Provide a safe and structured environment  Requests a family member to accompany client if he wanders around  Keep bed in low position  Provide adequate lightning  Assign consistent caregivers

ALZHEIMER S disease
5. Encourage exercise to maintain mobility

PARKINSON s Disease


A slowly progressing neurologic movement disorder The degenerative idiopathic form is the most common form

a chronic, slowly progressive disease of the nervous system that affects muscle movement. originates deep in the brain s substantia nigra area

substantia nigra area 400,000 special nerve cells

produce the chemical dopamine signal the body for proper muscle control and coordination

these cells are slowly destroyed, causing dopamine production to decrease & the signals to become chaotic

PARKINSON s Disease
Pathophysiology  Decreased levels of dopamine due to destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia  Clinical symptoms do not appear until 60% of the neurons have disappeared

PARKINSON s Disease
CLINICAL MANIFESTATIONS  1. Tremor- resting, pill-rolling  2. Rigidity- cog-wheel, lead-pipe  3. Bradykinesia- abnormally slow movement  4. Dementia, depression, sleep disturbances and hallucinations  5. excessive sweating, paroxysmal flushing, orthostatic hypotension

SIGNS & SYMPTOMS

1. Tremors - involuntary movements during muscular inactivity are a classic sign. 2. Muscular rigidity and Bradykinesia stiff muscles slow spontaneous movements
- Simple activities such as tying shoes and rising from a chair become a challenge; Stiffness also can affect the fine muscles of speech, swallowing, and respiration; may slur his words, stutter, speak in a whisper or a raspy voice, or lose his ability to speak altogether - swallowing difficulties that pose a risk of choking and the potential for aspiration pneumonia -If respiratory muscles stiffen, patient may have trouble breathing.

SIGNS & SYMPTOMS

3. Postural instability - a loss of coordination & balance can cause clumsy movements - With a stooped posture and a slow, shuffling gait, the patient may even appear intoxicated; when he s walking, he may unintentionally speed up his pace or his leg muscles might suddenly freeze without warning, causing him to lose balance and fall. 4. Changes in other body systems - affect almost all body systems including autonomic nervous system - patient may develop emotional changes, insomnia, a blank facial expression known as the mask of Parkinson s depression, dementia, constipation, and urinary problems - may have increased sweating, changes in temperature regulation, and skin flushing

PARKINSON s Disease
Medical management  1. Anti-parkinsonian drugs- Levodopa, Carbidopa  2. Anti-cholinergic therapy  3. Antiviral therapy- Amantadine  4. Dopamine Agonists- bromocriptine and Pergolide, Ropirinole anmd Pramipexole

PARKINSON s Disease
   

Medical management 5. MAOI 6. Anti-depressants 7. Antihistamine

TREATMENT

I. Drug therapy A. Sinemet (carbidopa-levodopa): is available in standard & controlledrelease forms;has been the cornerstone of therapy. It works by replacing dopamine in a form the brain can use. The downside of this therapy is that symptoms are under control during peak concentrations but might suddenly reappear as the drug wears off Higher doses of Sinemet counteract the on-and-off effects, but they can cause disturbing effects such as muscle twitching, jerking, and hallucinations B. Anticholinergics Artane (trihexyphenidyl) and Cogentin (benztropine): are commonly used in conjunction with Sinemet to help control tremor, rigidity, and excessive sweating. C. Dopamine agonists - mimic dopamine and may be used in conjunction with Sinemet
Recent studies show that Mirapex and Requip can reduce Parkinson symptoms and delay disease progression

TREATMENT

D. COMT (catechol Omethyltransferase) -inhibitors block the breakdown of levodopa in the body so more can travel to the brain and convert to dopamine; Used in conjunction with Sinemet, they help prevent wearing off periods. Tasmar (tolcapone) & Comtan (entacapone) are current COMT inhibitors. II. Surgery III. Deep-brain stimulation works by sending precise impulses to offending brain areas to slow chaotic brain signals, which, in turn, reduces slowness, shaking, and stiffness associated with the disease; unfortunately, this technique doesn t alleviate balance problems.

PARKINSON s Disease
      

NURSING INTERVENTIONS 1. Improve mobility 2. Enhance Self- care activities 3. Improve bowel elimination 4. Improve nutrition 5. Enhance swallowing 6. Encourage the use of assistive devices

PARKINSON s Disease
  

NURSING INTERVENTIONS 7. improve communication 8. Support coping abilities

NURSING CARE

1. Speech Listen closely to speech pattern. Is the patient s voice hoarse or hard to hear? Does he mumble or slur his words? If any of these conditions exists, he may need evaluation by a speech therapist Assess him for dysphagia and determine the best way for him to receive nutrients Use the nursing care plan to advise staff about the best way to communicate with him and to describe his limitations Observe him carefully during meals and document any difficulties you identify 2. Nutrition If the patient appears thin or malnourished, he may be suffering from dysphagia A dietitian can order a calorie count and suggest lab tests, such as a prealbumin level, to determine his nutritional status

Discuss what he likes to eat at home. Because elderly Parkinson s patients may have decreased gastric acid and gastric motility problems, assess for vitamin/mineral deficiencies, especially vitamin B or iron deficiencies Give daily multivitamin/mineral because these supplements will decrease the availability of levodopa in his system, he should take them at least 2 hours apart. 3. Physical capabilities Assess the patient if they have balance problems or a history of falls; if they need assistance with activities of daily living; if so, ask his doctor to order a physical or occupational therapy evaluation  Be sure to identify him as high risk for falls and encourage him to call for assistance before trying to get out of bed 4. Drug therapy effectiveness Ensure the patient continues to receive his Parkinson s medication while he s hospitalized;Ask for any periods when his medication wears off.

EPILEPSY
A group of syndromes characterized by recurring seizures CAUSES 1. idiopathic 6. brain tumors 2. Birth trauma 7. head Injury 3. perinatal infection 8. metabolic disorders 4. infectious disease 9. CVA 5. ingestion of toxins


 also known as seizure disorder;a brain condition characterized by recurrent seizure

SEIZURES are paroxysmal events associated with abnormal electrical discharges of neurons in the brain  the discharge may (a) trigger a convulsive movement (b) an interruption of sensation, (c) an alteration in level of consciousness or a combination of these symptoms

 in most patients,epilepsy does not affect intelligence  this condition is probably present in 0.5% to 2% of the population & usually occurs in people under age 20.  about 80% of patients have good seizure control with strict adherence to prescribed treatment

Neurons lose afferent stimulation

CAUSES:  50% of epileptic case are idiopathic no specific cause and patient has no Other neurologic abnormality  other causes:
Epileptogenic focus becomes hypersensitive & easily activated Increase permeability of the cytoplasmic membranes causes neurons fire abnormally Seizure discharges will spreads to adjacent brain areas Involve the motor, sensory & autonomic responses

genetic abnormalities such as Tuberous sclerosis & phenylketonuria perinatal injuries metabolic abnormalities such as hyponatremia,hypocalcemia,pyridoxine deficiency & hypoglycemia brain tumors or other space occupying lesions of the cortex infections traumatic injury esp. if the dura mater has been penetrated ingestion of toxins such as mercury, lead,carbon monoxide fever stroke

A, Normally, excitatory messages from the cerebral cortex are modulated by deeper structures. B, In clients with epilepsy, bursts of activity from the cortex are not modulated and these bursts spread.

EPILEPSY


Recurring seizures may be classified as GENERALIZED or PARTIAL SEIZURES Generalized Seizures- cause a generalized electrical abnormality within the brain Partial seizures- these seizures arise from a localized part of the brain and cause specific symptoms

TYPES OF SEIZURE /SIGNS & SYMPTOMS 1. Generalized seizures 3. Memory loss during & immediately after seizure

a. Tonic-clonic: stiffening or rigidity of Muscles lasting 10-20 seconds 4. Drowsiness or difficulty with arousal for b. Focal seizure: slow, repetitive jerking short period of time following seizure of a body part 5. Incontinence of urine or feces c. Absence seizures: (petit mal) sudden 6. Vomiting Brief cessation of all motor activity 7. Hypoxia (severe prolonged seizures) Accompanied by a blank stare d. Myoclonic brief, generalized jerking of 8. Automatism (lip smacking,repeated extremities swallowing) e. Atonic: (drop attacks) sudden, Momentary loss of muscle tone 2. Partial seizures a. Simple: conscious with localized jerking of specific area b. Complex: momentary loss of consciousness with periods of unintentionally altered behavior

GENERALIZED SEIZURES


1. General Tonic-Clonic seizure- (Grand mal) characterized by loss of consciousness and alternating movements of the extremities 2. Absence Seizure (Petit mal)- common in children, begins with a brief change in the LOC, indicated by blinking, rolling of eyes and blank stares

GENERALIZED SEIZURES


3. Myoclonic seizure- characterized by brief, involuntary muscular jerks of body extremities 4. Akinetic seizure- general loss of postural tone and a temporary loss of consciousness- a drop attack

PARTIAL SEIZURES


1. Simple partial seizure- typically limited to one cerebral hemisphere 2. Complex partial seizure- begins with an aura, then with impaired consciousness, with purposeless behaviors like lip-smacking, chewing movements

TYPES OF SEIZURE /SIGNS & SYMPTOMS 1. Generalized seizures 3. Memory loss during & immediately after seizure

a. Tonic-clonic: stiffening or rigidity of Muscles lasting 10-20 seconds 4. Drowsiness or difficulty with arousal for b. Focal seizure: slow, repetitive jerking short period of time following seizure of a body part 5. Incontinence of urine or feces c. Absence seizures: (petit mal) sudden 6. Vomiting Brief cessation of all motor activity 7. Hypoxia (severe prolonged seizures) Accompanied by a blank stare d. Myoclonic brief, generalized jerking of 8. Automatism (lip smacking,repeated extremities swallowing) e. Atonic: (drop attacks) sudden, Momentary loss of muscle tone 2. Partial seizures a. Simple: conscious with localized jerking of specific area b. Complex: momentary loss of consciousness with periods of unintentionally altered behavior

A, The tonic phase of a seizure is marked by loss of consciousness, falling, crying, and generalized stiffness. There may be incontinence. B, During the clonic phase, there is jerking of the limbs and salivary frothing.

DIAGNOSTIC TESTS 1. History & physical exam 2. Blood & urine tests 3. MRI (Magnetic Resonance Imaging) 4. CT (Computed tomography) scan 5. EEG (Electroencephalogram) 6. CSF (Cerebrospinal fluid) analysis 7. Skull x-rays 8. Electrolyte profile 9. Drug screen PHARMACOLOGY 1. 2. Anticonvulsants (phenytoin,valproic acid,phenobarbital,carbamazepine) Sedatives(benzodiazepines) 1. 2. 3. 4. 5. 6.

COMPLICATIONS Disruption in attention span Intereference with learning Injury Aspiration Alteration in self-concept Status epilepticus

Epilepsy
     

DIAGNOSTIC TESTS 1. EEG 2. CT 3. MRI 4. LP 5. Angiography

Epilepsy
 

Medical treatment 1. Anticonvulsants- most commonly phenytoin, phenobarbital and carbamazepine Ethosuximide and valproic acid for absence seizure 2. surgery

Epilepsy
   

Nursing Intervention 1. Care of patients during seizure 2. care of patients after seizures 3. patient teaching

NURSING MANAGEMENT e. Administer oxygen 1. Prevent: f. Minimize stimuli in environment during a. Seizures by maintaining medication Seizure schedules g. Administer prescribed medications b. Injury h. Alleviate anxiety c. Aspiration i. Identify factors that trigger seizures 2. Assess / monitor: j. Document time & duration of seizure a. Airway & breathing k. Teach client to avoid alcohol, excessive b. During & following seizure fatigue & stress l. Refer to appropriate community resources 3. Nursing activities: m. Encourage verbalization of fears & a. maintain patent airway concerns b. Turn client s head to side & prepare to suction c. Loosen restrictive clothing but do not Physically restrain d. Protect client from injury (padded side ails, place standing client on floor & protect head & body)

BELL S PALSY
    

Causes 1. infection 2. hemorrhage 3. tumor 4. local traumatic injury

BELL S PALSY
       

MANIFESTATIONS 1. Unilateral facial weakness 2. Mouth drooping 3. Distorted taste perception 4. Smooth forehead 5. Inability to close eyelid on the affected side 6. Incomplete eye closure 7. excessive tearing when attempting to close the eyes 8. Inability to raise eyebrows, puff out the cheek

BELL S palsy
    

Diagnostic tests EMG Medical management 1. Prednisone 2. Artificial tears

BELL S palsy
  

 

Nursing Interventions 1. Apply moist heat to reduce pain 2. Massage the face to maintain muscle tone 3. Give frequent mouth care 4. protect the eye with an eye patch. Eyelid can be taped at night 5. instruct to chew on unaffected side

Trigeminal neuralgia
 

Also called Tic Douloureux Painful disorder that affects one or more branches of the fifth cranial nerve CAUSES: repetitive pulsation of an artery as it exits the pons is the usual cause

Trigeminal neuralgia
  

ASSESSMENT 1. Pain history 2. Searing or burning jabs of pain lasting from 1-15 minutes in an area innervated by the trigeminal nerve DIAGNOSTIC TESTS Skull x-ray or CT scan

Trigeminal neuralgia
   

NURSING INTERVENTIONS 1. provide emotional support 2. encourage to express feelings 3. provide adequate nutrition in small frequent meals at room temperature

Myasthenia gravis


A sporadic, but progressive weakness and abnormal fatigability of striated muscles which are exacerbated by exercise and repetitive movements

Myasthenia gravis
ETIOLOGY  Autoimmune disease  Thymoma Women suffer at an earlier age and are more affected

Myasthenia gravis
Pathophysiology:  1. Acetylcholine receptor antibodies interfere with impulse transmission  2. Follows an unpredictable course of periodic exacerbations and remissions

Myasthenia gravis
CAUSE: autoimmune disorder that impairs transmission of nerve impulses ASSESSMENT FINDINGS 1. Gradually progressive skeletal muscle weakness and fatigue 2. Weakness that worsens during the day 3. Ptosis, diplopia and weak eye closure 4. Blank, mask-like facies 5. Difficulty chewing and swallowing 6. Respiratory difficulty


Myasthenia gravis
DIAGNOSTIC TESTS  1. EMG  2. TENSILON TEST  3. CT scan  4. Serum anti-AchReceptor antibodies

Myasthenia gravis
MEDICAL THERAPY  Anticholinesterase drugspyridostigmine and neostigmine  Corticosteroids  Immunosuppresants  Plasmapheresis  Thymectomy

Myasthenia gravis
NURSING INTERVENTIONS  1. Administer prescribed medication as scheduled  2. Prevent problems with chewing and swallowing  3. Promote respiratory function  4. Encourage adjustments in lifestyle to prevent fatigue  5.maximize functional abilities

Myasthenia gravis


 

6. Prepare for complications like myasthenic crisis and cholinergic crisis 7. prevent problems associated with impaired vision resulting from ptosis of eyelids 8. provide client teaching 9. promote client and family coping

Meningitis


Infection or inflammation of the meninges covering the brain and spinal cord. Caused by bacterial, viral and fungal agents

 brain & spinal cord meninges become inflamed that involve all membranes: the dura mater, the arachnoid membrane and the pia mater and the underlying cortex  prognosis for patients with meningitis is good & complications are rare especially if the disease is recognized early & the infecting organism responds to antibiotics Bacterial (Neisseria meningitidis,Haemophilus influenzae, Streptococcus pneumonia,Escherichia coli);Viral;Protozoal;Fungi Blood flow to the brain is reduced Brain tissues swell Increase intracranial pressure

2 TYPES 1. BACTERIAL
 affect infant & children

2. VIRAL
 caused by a virus is called aseptic viral meningitis  may result from a direct infection or Secondary to disease such as mumps, Herpes, measles or leukemia  symptoms are mild & the disease is self limiting

 secondary to another bacterial Infection:bacteremia,sinusitis,otitis Media,encephalitis,myelitis or brain abscess  it may also follow skull fracture, a penetrating head wound, lumbar puncture or ventricular shunting procedures SIGNS/SYMPTOMS: Restlessness Headache Nuchal rigidity Chills & high fever Photophobia
Seizures Increase ICP Back & abdominal pain Twitching Coma

SIGNS/SYMPTOMS:
Mild, flu like symptoms Intense headache malaise nausea/vomiting drowsiness Nuchal rigidity Low grade fever

DIAGNOSTIC & LABORATORY TESTS: 1. History & physical examination

4. Chest X-ray are important because they may reveal pneumonitis or lung abscess, tubercular lesions, or granulamous secondary to fungal infection

2. Vision tests may show diplopia & other 5. Sinus and skull x-ray may help identify Visual problems The presence of cranial osteomyelitis, Paranasal sinusitis or skull fracture 6. WBC count usually indicates leukocytosis And abnormal serum electrolyte levels. 7. CT scan rules out cerebral hematoma, Hemorrhage or tumor 8. Positive Kernig s sign 3. Lumbar puncture shows elevated CSF Pressure, cloudy or milky CSF, a high CHON 9. Positive Brudzinski s sign Level, positive gram stain & culture that Usually identifies the infecting organism (unless it is a virus) & depressed CSF Glucose concentration

One of the physically demonstrable symptoms of meningitis is Brudzinski's sign;Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed

One of the physically demonstrable symptoms of meningitis is Kernig's sign. Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees

TREATMENT:

COMPLICATIONS:

1. Seizures 1. Medications: 2. Airway obstruction & respiratory  IV antibiotics for 2 weeks followed arrest by oral antibiotics:penicillin G,ampicillin, 3. Cardiac dysrhythmias or nafcillin; tetracycline chloramphenicol 4. Deafness or kanamycin 5. Shock  Anticonvulsant,antipyretics,analgesics 6. Dehydration 7. Death  Antipyretics & analgesics  digitalis glycoside: digoxin to control Arrhythmias  Mannitol to decrease cerebral edema 2. Supportive measures  Bed rest  Hypothermia  Fluid therapy to prevent dehydration  Isolation is necessary if nasal culture are positive

THERAPEUTIC NURSING MANAGEMENT 1. Assess / Monitor: a. Neurological status frequently b. Vital signs, especially temperature c. Level of consciousness d. For signs of seizure activity e. Signs of increase ICP (decrease pulse rate & respiration,BP & temperature increases,widening pulse pressure ) f. Intake & output g. dehydration 2. Implement fever reduction measures if necessary 3. Maintain client safety (padded side Rails,oral airway bedside) 4. Administer medications 5. Maintain respiratory isolation until antibiotics have been administered 6. Report seizure activity

Brain Abscess


A free or encapsulated collection of pus in the brain parenchyma Causes: usually secondary to another infection like- sinusitis, meningitis, dental abscess, mastoiditis, bacteremia and trauma

Encephalitis


Intense inflammation of the brain tisssue with lymphocytic infiltration, cerebral edema, degeneration of brain cells and diffuse nerve cell destruction

CNS infections
      

ASSESSMENT FINDINGS Meningitis 1. fever, headache, vomiting 2. positive meningeal sings Brain abscess 1. headache, N/V, seizures, changes in LOC 2. Focal neurologic deficits

CNS infections
       

DIAGNOSTIC TESTS 1. CT scan 2. MRI 3. EEG MEDICAL TREAMENT 1. Antibiotics 2. Surgical drainage 3. Drugs to reduce increased ICP

CNS infections
 

  

NURSING INTERVENTIONS 1. Frequent monitoring of neurologic status 2. Monitor intake and output 3. Administer antibiotics 4. Administer mild laxative to prevent constipation 5. maintain quiet environment

Neoplastic diseases


A brain tumor is a localized intracranial lesion that occupies space within the skull Primary brain tumors originate from cells and structures within the brain.

Neoplastic disease
 

The cause of brain tumors is unknown The only risk factor accepted is radiation exposure to ionization rays

Neoplastic disease
 

CLINICAL MANIFESTATIONS 1. increased ICP

   

Vomiting Headache. Especially early in the morning Vomiting Visual disturbances

Neoplastic disease
   

2. Localized symptoms Hemiparesis Seizures Mental status changes

Neoplastic disease
    

DIAGNOSTIC TESTS 1. CT scan 2. MRI 3. PET 4. EEG

Neoplastic disease
   

MEDICAL MANAGEMENT Surgery Chemotherapy Radiotherapy

Neoplastic disease
     

NURSING INTERVENTIONS 1. promote self-care independence 2. improve nutrition 3. relieve anxiety 4. enhance family processes 5. provide pre-operative and post-operative care 6. manage pain

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