NEURO DISORDERS

• Infectious Neurological Disorders

  • Meningitis
  • Brain Abscess
  • Encephalitis
• Meningitis


  Inflammation of meninges
• Types of Meningitis

  • Bacterial
  • Viral
• Causes of Septic Meningitis

  • Streptococcus Pneumoniae
  • Neisseria Meningitis
• Causes of Aseptic Meningitis

  • Viral
  • Secondary to Cancer
  • Weakened immune system like Human Immunodeficiency Virus (HIV)
• Pathophysiology of Meningitis

  1. Bacteria enters blood stream/ direct spread (trauma)

  2. Enters the mucosal surface/ cavity

  3. Breakdown of normal barriers

  4. Crosses the blood brain barrier

  5. Proliferates in the CSF

  6. Inflammation of the Meninges

  7. Increase ICP
• Symptoms of Meningitis

  • Fever
  • Headache
  • Stiff neck
  • Sensitivity to light (photophobia)
  • Nausea and vomiting
  • Confusion (altered mental state)
• Clinical Manifestations of Meningitis

  • Headache along with fever and chills are frequently initial symptoms
  • Neck immobility – nuchal rigidity (stiff and painful neck – early sign)
  • Positive Kernig Sign
  • Positive Bruzinski
  • Photophobia
  • Rash – striking feature of M. Meningitidis
• Diagnostic Tests for Meningitis

  • CT Scan
  • Bacterial Culture and Gram Staining of CSF and Blood
  • Eye exam
  • Ear exam
  • Blood test
  • Lumbar puncture
  • EEG
  • MRI or X-ray
• Medical Management of Meningitis

  • Penicillin G + Cephalosphorins
  • Dexamethasone
  • Fluid volume expanders
  • Anticonvulsants
• Nursing Management of Meningitis

  • Enforce respiratory isolation for 24 hours after initiation of antibiotics
  • Provide bed rest. Keep room dark and quiet
  • Administer analgesics for headache as prescribed
  • Maintain fluid and electrolyte balance
  • Monitor vital signs and neuro VS frequently
  • Diet: high calorie, high protein, small frequent feeding
  • Monitor daily body weight
  • Implement interventions to treat elevated temperature
  • Protect the patient from injury secondary to seizure activity
  • Prevent complications associated with immobility, such as pressure injury and pneumonia
• Brain Abscess


  Pus-filled pocket of infected material in the brain
• Brain abscesses are frequently diagnosed in people who are immunosuppressed as a result of an underlying disease
• Pathophysiology of Brain Abscess

  1. Bacteria are the most common causative organism

  2. Otogenic in origin (otitis media and rhinosinusitis)

  3. Abscess can result from intracranial surgery, penetrating head injury, or piercing

  4. Organisms may reach the brain by hematologic spread

  5. Inflammation/ increase ICP
• Diagnostic Tests for Brain Abscess

  • CT Scan with contrast
  • Culture and Sensitivity of Abscess by means of aspiration guided by CT or MRI
  • Blood cultures
• Clinical Manifestations of Brain Abscess

  • Alteration in-intracranial dynamics (edema, brain shift, infection, or location of the abscess)
  • Headache - usually worse in the morning
  • Mental status changes
  • Elevated body temperature
  • Vomiting and focal neurologic deficits
  • Decreasing LOC
  • Seizures
• Medical Management of Brain Abscess

  • Ceftriaxone + Metronidazole
  • Corticosteroids - reduce inflammatory cerebral edema
  • Anticonvulsant - prevent or treat seizure
• Nursing Management of Brain Abscess

  • Assess neurologic status
  • Administer medications
  • Assess response to treatment
  • Provide supportive care
  • Blood laboratory tests results, (blood glucose potassium) are closely monitored when corticosteroids are prescribed
  • Injury may result in decreased LOC or falls related to motor weakness or seizure
  • Obtain support
• Encephalitis


  Acute inflammatory process of the brain tissue
• Causes of Encephalitis

  • Herpes Simplex Virus (most common)
  • Fungi (Cryptococcus Neoformans)
  • Arthropod-borne Virus
• Encephalitis involves local necrotizing hemorrhage that becomes more generalized, followed by edema, and progressive deterioration of nerve cell bodies
• Diagnostic Tests for Encephalitis

  • EEG - diffuse slowing or focal changes
  • CSF Examination by means of lumbar puncture
  • MRI - detect inflammation
  • PCR - standard test for dx of herpes simplex encephalitis (DNA bands of HSV-1 in CSF)
• Clinical Manifestations of Encephalitis

  • Headache along with fever, confusion and hallucinations are frequent presenting symptoms
  • Nuchal rigidity
  • Confusion
  • Decreased LOC
  • Seizure
  • Sensitivity to light
• Management of Encephalitis

  • Antiviral agent-Acyclovir (inhibition of viral DNA replication)
  • Assessment of the neurologic function
  • Comfort measures to reduce headache
  • Injury prevention and safety
  • Urinary output monitoring
• Arthropod-borne Virus Encephalitis


  Maintained in nature through biologic transmission between susceptible vertebrae hosts by blood feeding arthropods
• Diagnostic Tests for Arthropod-borne Virus Encephalitis

  • EEG-identify abnormal brain waves
  • CSF Examination by means of lumbar puncture
  • MRI-demonstrates inflammation
• Clinical Manifestations of Arthropod-borne Virus Encephalitis

  • Flulike symptoms-headache along with fever
  • SIADH with hyponatremia unique clinical feature of arboviral encephalitis
  • Arboviral infections are seasonal (summer or fall)
• Management of Arthropod-borne Virus Encephalitis

  • NO specific medication exists
  • Injury prevention is key in light of the potential for fall or seizure
  • Assess neurologic status and identify improvement or deterioration in patient's condition
  • Clothing that provides coverage and insect repellents
  • Remaining indoors
  • Report cases to the local health department
• Autoimmune Disorders

  • Multiple Sclerosis
  • Myasthenia Gravis
  • Guillain-Barre Syndrome
• Multiple Sclerosis


  Immune-mediated, progressive demyelinating disease of the CNS
• Multiple Sclerosis is chronic, progressive, characterized by periods of mission and exacerbation
• Causes of Multiple Sclerosis

  • Unknown
  • Post Viral Infection
• Pathophysiology of Multiple Sclerosis

  1. Sensitized T and B lymphocytes cross the blood-brain barrier- checking the CNS for antigens and then leave

  2. Sensitized T cells remain in the CNS

  3. Promote Infiltration of other agents that damage the immune system

  4. Immune system attack leads to inflammation that destroys mostly the white matter of the CNS
• Diagnostic Tests for Multiple Sclerosis

  • MRI-identify presence of plaques
  • Electrophoresis of CSF identifies presence of oligoclonal banding
  • Evoked Potential Studies - define extent of the disease process
• Clinical Manifestations of Multiple Sclerosis

  • Scanning Speech
  • Intentional Tremors
  • Nystagmus
  • Visual: blurring of vision, diplopia, total blindness
  • Sensory: paresthesia, pain
  • Cognitive: memory loss, dementia, decreased concentration
  • Cerebellum/Basal Ganglia: tremors, ataxia
  • Bowel and bladder dysfunction
• Management of Multiple Sclerosis

  • Interferon Beta-1a and Interferon Beta-2B
  • Methylprednisolone-anti-inflammatory effects
  • Baclofen - treat spasticity
  • Beta Blockers, Anticonvulsant, Benzodiazepines - treat ataxia
• Nursing Management of Multiple Sclerosis

  • Promote physical mobility (walking, use of assistive devices)
  • Warm packs (minimizes spasticity of contractures)
  • Avoid hot bath (increases risk for bum injury)
  • Swimming and stationary bicycling are useful in treating spasticity
  • Strenuous exercises are to be avoided
  • Instruct client to prevent cuts and burns
  • Eye patch for diplopia
  • Respiratory distress precautions
  • Bowel and bladder program
• Myasthenia Gravis


  Autoimmune disorder affecting the myoneural junction, characterized by varying degrees of weakness of the voluntary muscles
• Myasthenia Gravis is characterized by a deficiency in acetylcholine due to increased acetylcholine destruction
• Pathophysiology of Myasthenia Gravis

  1. Chemical impulse precipitates the release of acetylcholine from vesicles on the nerve terminal at the myoneural junction

  2. The acetylcholine attaches to the receptor sites on the motor endplate and stimulates muscle contraction

  3. Antibodies directed at the acetylcholine receptor sites impair transmission of impulses across the myoneural junction

  4. Fewer receptors are available for stimulation, resulting in voluntary muscle weakness that escalates with activity