CCN NERVOUS SYSTEM

ROLI JOSEPH Z MONTA

Skull: Frontal, Parietal, Temporal, Occipital bones
Meninges: Dura Mater, Arachnoid layer, Pia Mater
Cerebrospinal Fluid (CSF): clear, colorless fluid, fluid shock absorber
Cerebral Vasculature: receives 20% of the cardiac
output approx. 750ml/min
Brain: cerebrum, pons, medulla and cerebellum
Spinal Cord: 33 vertebrae (7 Cervical, 12 Thoracic, 5 Lumbar, 5 Sacral
fused into one, 4 Coccygeal fused into one)

CENTRAL NERVOUS SYSTEM (CNS)

SPINAL NERVES
31 Pairs
8 Cervical
12 Thoracic
5 Lumbar
5 Sacral
1 Coccygeal

PERIPHERAL NERVOUS SYSTEM

 CRANIAL NERVE TRACT FUNCTION LOCATION OF ORIGIN
I. OLFACTORY SENSORY SENSE OF SMELL DIENCEPHALON
II. OPTIC SENSORY VISION DIENCEPHALON
III. OCULOMOTOR PARASYMPATHETIC PUPILLARY CONSTRICTION MIDBRAIN
MOTOR ELEVATION OF UPPER EYELID AND 4 OF 6 EXTRAOCULAR
MOVEMENTS
IV. TROCHLEAR MOTOR DOWNWARD, INWARD MOVEMENT OF THE EYE MIDBRAIN
(SUPERIOR OBLIQUE)
V. TRIGEMINAL MOTOR MUSCLES OF MASTICATION AND OPENING JAW PONS
SENSORY TACTILE SENSATION TO CORNEA, NASAL, ORAL MUCOSA AND
FACIAL SKIN
VI. ABDUCENS MOTOR LATERAL DEVIATION OF EYE PONS
VII. FACIAL PARASYMPATHETIC SECRETORY FOR SALIVATIONS AND TEARS PONS
MOTOR MOVEMENT FACIAL EXPRESSIONS, CLOSE EYE
SENSATION OF EXT EAR, AUDITORY CANAL, TYMPHANIC
SENSORY MEMBRANE
TASTE SENSATION ANTERIOR 2/3 OF TONGUE
VIII. VESTIBULOCOCHLEAR SENSORY Vestibular branch: Equilibrium PONS
(ACOUSTIC/COCHLEAR) Cochlear: Hearing
IX. GLOSSOPHARYNGEAL PARASYMPATHETIC SALIVATION MEDULLA
MOTOR VOLUNTARY MUSCLES FOR SWALLOWING AND PHONATION
SENSATION TO PHARYNX, SOFT PALATE, AND POSTERIOR 1/3
OF TONGUE
SENSORY STIMULATION ELICITS GAG REFLEX
 CRANIAL NERVE TRACT FUNCTION LOCATION OF ORIGIN

X. VAGUS PARASYMPATHETIC AUTONOMIC ACTIVITY OF VISCERA OF THORAX AND MEDULLA

ABDOMEN
MOTOR INVOLUNTARY ACTIVITY OF VISCERAL MUSCLES OF
HEART, LUNGS AND DIGESTIVE TRACT
INNERVATION OF STRIATED MUSCLES OF SOFT
PALATE, PHARYNX, LARYNX FOR VOLUNTARY
SWALLOWING

SENSORY SENSATION TO THE AUDITORY CANAL, PHARYNX,

LARYNX, AND VISCERA OF THORAX AND ABDOMEN
XI. SPINAL MOTOR STERNOCLEIDOMASTOID AND TRAPEZIUS MUSCLE MEDULLA
MOVEMENTS
XII. HYPOGLOSSAL MOTOR TONGUE MOVEMENTS MEDULLA

PERIPHERAL NERVES
NOCICEPTORS
- pain receptors that are stimulated and send impulses back to the
spinal cord then to the brain as a result of damaged tissue
- stimulation of nociceptors is caused by the release of substances from
damaged tissue and activation of inflammatory response
- damaged cells release potassium and hydrogen ion, both of which can
stimulate nociceptors
- Inflammatory cells: macrophages, neutrophils, other WBCs
- Platelets participating in clot formation release serotonin, also
stimulates nociceptors

PAIN
REFERRED PAIN
- pain perceived as arising from a site that is different from its true point of origin
- the “true point of origin” is from visceral organ or deep somatic structure
- the “point of reference” is some area of the body surface
- the most generally accepted theory for referred pain is that the 2 sensory
neurons, one from the region of the true point of origin and one from the point
of reference, enter the same segment of the spinal cord and synapse with the
same projection neuron
- Referring pain from SEVERE CARDIAC ISCHEMIA to the left arm or the referring
of DIAPHRAGMATIC PAIN to the neck and shoulder

PAIN
MENTAL STATUS
Alert (full consciousness): normal
Awake: fully oriented when aroused
Lethargic: drowsy but follows simple commands when stimulated
Obtunded: arousable with stimulation; responds verbally with a word or two;
follows simple commands; otherwise drowsy
Stuporous: very hard to arouse; inconsistently may follow simple commands or
speak single words or short phrases; limited spontaneous movement
Semicomatose: movements are purposeful when stimulated; does not follow
commands or speak coherently
Comatose: may respond with replexive posturing when stimulated or may have
no response to any stimulus

PATIENT ASSESSMENT
MENTAL STATUS
GCS: EMV
AVPU: Alert, Verbal, Pain, Unconscious

MOTOR FUNCTION
Motor responses to Pain

Pupillary Changes
PERRLA, Pupils Equal, Round, Reactive to Light and Accomodation
- in millimeter (mm)
- pupils size and shape
- Anisocoria
Pinpoint pupils: Drugs (opiates), Drops (meds for glaucoma), “Nearly dead”
(damage in the pons area of the brain stem)
Dilated Pupils: Fear (panic attack, extreme anxiety), “Fits” (seizure), “Fast Living”
(cocaine, crack, phenycyclidine)

CRANIAL NERVE FUNCTION

Nerve I, II, III, V, VII, IX, X (quick screening test for CN function) – ASSIGNMENT!
PATIENT ASSESSMENT
MOTOR FUNCTION
Motor responses to Pain

Finger to Nose Test – is performed by having the patient touch one finger to the
examiner’s finger, then touch his or her own nose
- overshooting or past-pointing the mark is called DYSMETRIA.
- Both sides are tested individually

Pronator Drift – have the patient hold the arms straight out with palms upward
and eyes closed and observe for any untoward drift or pronation of the forearms

Oculocephalic Reflex – indicates an intact brainstem

- this maneuver must not be performed in a person with
possible cervical spine injury

PATIENT ASSESSMENT
REFLEXES: Deep Tendon Reflex – 0 to 4 scale (2+ is Normal)
Plantar Reflex – Babinski’s sign is abnormal ; lesion in pyramidal tract
- but normal in children under the age of 2

Hyperreflexia is associated with upper motor neuron disease

Areflexia or absence of reflexes is associated with lower motor neuron
dysfunction

PATIENT ASSESSMENT
SENSATION
Proprioception is tested by asking the patient, with eyes closed to identify the
direction of the movement of finger in both extremities

Agnosia is the inability to recognize objects by touch, sight, or sound

Stereognosis is the ability to recognize and identify objects by touch
- is a function of the parietal lobe
Graphesthesia is the ability to recognize numbers or letters traced lightly on the
skin

PATIENT ASSESSMENT
 VITAL SIGNS
Respirations:
Cheyne-Stokes respirations (crescendo-decrescendo respirations alternating with
periods of apnea)
Hypoventilation can lead to respiratory acidosis
Hyperventilation after cerebral trauma produces respiratory alkalosis with
decreased blood CO2 levels
Shallow, rapid respirations can indicate a problem with maintenance of a patent
airway or the need for suctioning
Snoring respirations or stridor can indicate a partially obstructed airway

PATIENT ASSESSMENT
 VITAL SIGNS
Temperature (hypothalamus)
Hypothermia occurs with metabolic causes, pituitary damage and spinal cord
injuries
CNS fevers may be very high and differentiate themselves from other causes
of fever by their resistance to antipyretic therapy

Pulse – Tachycardia in increased ICP, alterations in ecg pattern such as atrial or

ventricular dysrhythmias

Blood Pressure (medulla)

Hypertension is common due to increase in ICP
Hypotension must be avoided in the post-injury stage because it can lead to
decreased cerebral perfusion, hypoxia and extension of the initial injury

PATIENT ASSESSMENT
Signs of Trauma and Infection
Battle’s sign (bruising over the mastoid areas) suggests a basilar skull fracture
Raccoon’s eye (periorbital edema and bruising) suggests a frontobasilar fracture
Rhinorrhea (drainage of CSF from the nose) suggest fracture of the cribriform plate with
herniation of a fragment of the dura and arachnoid through the fracture
Otorrhea (drainage of CSF from the ear) usually is associated with fracture of the petrous
portion of the temporal bone

Signs of Meningeal Irritation: nuchal rigidity (pain and resistance to neck flexion)
- fever, headache and photophobia
Kernig’s sign – pain in the neck when the thigh is flexed on the abdomen and the leg is
extended at the knee; meningitis inflammation
Brudzinski’s sign – involuntary flexion of the hips when the neck is flexed toward the
chest; meningitis inflammation

PATIENT ASSESSMENT
Signs of Increased Intracranial Pressure (ICP):
1. Decreased level of consciousness (LOC)
- restlessness, confusion and combativeness
- from lethargy, obtundation to coma
2. Pupillary reactions begins to diminish, with sluggishly reactive pupils and eventually
fixed, dilated pupils
- Frequently, because of the potential for injury to be ipsilateral, one pupil dilates before
the other one does, resulting in unequal pupils
3. Abnormal motor activity – from localized to painful stimuli to either abnormal flexion or
extension
4. Changes in vital signs

CUSHING’S TRIAD - increased systolic pressure (resulting in an increased pulse pressure),

bradycardia and irregular respirations, decreased pulse, pupillary changes
- a sign of impending herniation

PATIENT ASSESSMENT
Computed Tomography or CT Scan (Invasive and Noninvasive)
- a scanner takes a series of radiographic images all around the same axial plane.
A computer hen creates a composite picture of various tissue densities visualized.
The images may be enhanced with the use of IV contrast dye
- Instruct the patient to lie flat on a table with the machine surrounding Patient
must remain immobile as possible
Magnetic Resonance Imaging (MRI) – a selected area of the patient’s body is
placed inside a powerful magnetic field
- it gives a more defined image of anatomical details and may diagnose small
tumors or early infarction syndromes
- is contraindicated in patient’s with previous surgeries where hemostatic or
aneurysm clips were implanted
- also contraindicated to cardiac pacemakers, prosthetic valves, bullet fragments,
and orthopedic pins
- procedure is very noisy
- must remove all metal objects
- use caution if patient is claustrophobic

NEURODIAGNOSTIC STUDIES
Positron Emission Tomography (PET); Single-Photon Emission Computed Tomography (SPECT) -
the patient either inhales or receives by injection radioactively tagged substances, such as
oxygen or glucose. A gamma scanner measures the radioactive uptake of these substances
and computer produces a composite image, indicating where the radioactive material is
located, corresponding to areas of cellular metabolism

- help diagnose abnormalities and behavioral disturbances, such as dementia and

schizophrenia, that may have a physiological basis

- the patient receives only minimal radiation exposure because the half-life of radionuclides
used is from a few minutes to 2 hours

-testing may take a few hours

- very expensive

- instruct the patient that remaining very still and immobile will produce best test results

NEURODIAGNOSTIC STUDIES
Cerebral Angiography (invasive)

- is a radiographic contrast study in which radiopaque contrast medium is injected by a

catheter into the patient’s cerebral arterial circulation.
- the contrast medium is directed into each common carotid artery and each vertebral artery,
and serial radiographs are then taken
- the contrast medium illuminates the structure of the cerebral circulation
- the vessel pathways are examined for patency, narrowing and occlusion
- the femoral artery is a common insertion site. Local anesthesia will be used
- a warm, flushed feeling will occur when the contrast medium is injected
- after the procedure, assess the puncture site for swelling, redness and bleeding. Also, check
the skin color, temperature, and peripheral pulses of the extremity distal to the site for signs
of arterial insufficiency (CTP)

NEURODIAGNOSTIC STUDIES
Electroencephalogram, or EEG (noninvasive)

- is a recording of electrical impulses generated by the brain cortex that are sensed by
electrodes on the surface of the scalp

- helps detect and localize abnormal electrical activity occurring in the cerebral cortex

- it aids in seizure focus detection, localization of a source of irritation such as a tumor or

abscess and diagnosis of metabolic disturbances and sleep disorders

- the patient’s scalp and hair should be free of dirt, creams, and sprays because they can cause
electrical interference and thus, an inaccurate recording (shampoo patient’s hair)

NEURODIAGNOSTIC STUDIES
LUMBAR PUNCTURE – fetal position
- a hollow needle is positioned in the subarachnoid space at L3-L4 or L4-L5 level, and CSF is
sampled
- the pressure of the CSF also is measured (45mm H2O in full term newborns – 120 mm H2O
in adults)
- the CSF is examined for blood and for alterations in appearance, cell count, protein and
glucose
- the test is contraindicated in patients with suspected increased ICP because a sudden
reduction in pressure from below may cause brain structures to herniate, leading to death
- in preparation for this test, position the patient on side with knees, and head flexed.
- Explain to the patient that some pressure may be felt as the needle is inserted and not to
move suddenly or cough
- After this procedure, keep the patient flat for 8-10 hours to prevent headache. Encourage
liberal fluid intake
- Complications from CSF leak include a postprocedure headache, nuchal rigidity, fever and
difficulty voiding. Treatment involves the injection of blood into the dura, called a Blood Patch,
to stop the leak
NEURODIAGNOSTIC STUDIES
Normal CSF Values:

Color colorless, clear

WBC 0-5 mm3, all mononuclear
RBC none
Chloride 120-130 mEq/L
Glucose 50-75 mg/100 ml
Pressure 70-180
Protein 14-45 mg/100 ml

NEURODIAGNOSTIC STUDIES
HYPEROSMOLAR THERAPY
Hypertonic Agents
Hypertonic Saline – induced hypernatremia has been demonstrated to increase
cerebral perfusion pressures and decrease intracerebral pressure in multiple
pathologies (stroke, subarachnoid hemorrhage, mass lesions)
- bolus dosing vs. continuous infusion
- 2% to 23.4%

Mannitol Administration – a hypertonic crystalloid solution that decerease cerebral

edema, is also used as first-tier therapy for reducing ICP after brain injury
- monotherapy, if combined with Furosemide, there is a risk for excessive diuresis,
causing depletion of intravascular urine and electrolytes
- foley catheter must be inserted
- BP precaution

CLINICAL MANAGEMENT
RESPIRATORY SUPPORT

- Normocapnia is essential for maintaining stable ICP because CO2 directly affectsthe degree of
vasodilation in the cerebral blood vessels

- limit the duration of passes of suction catheter to no more than 5-10 seconds avoids hypoxia

- limiting the number of passes to 1 or 2 avoids overstimulation of the cough reflex and
decreases the incidence of intrathoracic pressure and ICP

CLINICAL MANAGEMENT
Analgesics, Sedatives and Paralytics
In patients with severe brain injury, GCS Score < 8:
- reduce agitation, discomfort and pain
- facilitate mechanical ventilation by suppressing coughing
- limit responses to stimuli, such as suctioning

Analgesics – Opioid narcotics primarily affect the CNS

- Fentanyl and morphine
- Limit pain caused by injuries and nursing interventions
- Facilitate mechanical ventilation
- Potentiate the effect of sedatives
- adverse effects: respiratory depression, depression of the cough reflex, mood changes, nausea
and vomiting
- Naloxone (Narcan) reverses CNS depression (narco toxicity)

PHARMACOLOGICAL THERAPY
SEDATIVES
- Benzodiazepines
- Midazolam, Diazepam (Valium), Lorazepam before ICU procedures and as needed to treat
anxiety
- Lorazepam for alcohol withdrawal and anticonvulsant therapy
- Midazolam with Fentanyl is most often used before procedures

ANESTHETICS
Propofol is administered as continuous infusion to decrease agitation in the critically ill patient
- common side effect is Hypotension

BP Management
- MAP greater than 110 mm Hg must be avoided
- ACE inhibitors: Lisinopril
- B blockers:

PHARMACOLOGICAL THERAPY
SEIZURE PROPHYLAXIS

- 7 days use to decrease the incidence of early seizure

- Phenytoin, Levetiracetam and Carbamazepine
- Levetiracetam (Keppra) is more convenient to administer as no blood drug levels
need to be followed

PHARMACOLOGICAL THERAPY
CEREBROVASCULAR DISEASE (STROKE)
Causes: Thrombosis, Embolism, Hemorrhage
- damage to a focal area of the brain
- occurs when there is a disruption of blood flow to a region of the brain
- “brain attack”

Clinical Management
4 Goals:
1. Reperfusion
2. Prevention of recurrent thrombosis
3. Neuroprotection
4. Supportive care – emotional and behavioral modification, communication, rehabilitation

NEUROLOGICAL DISORDERS
Thrombus or Embolus:
- oxygen and substrate deprivation of the cerebral tissue begins
Deprivation for 1 minute – reversible symptoms, such as LOC
O2 deprivation for longer periods – microscopic necrosis of the neurons (infarcted)

Clinical Manifestations:
weakness, numbness, visual changes, dysarthria, dysphagia, or aphasia

Transient Ischemic Attack (TIA)

- neurological deficit lasting less than 24 hours that is attributed to focal or retinal ischemia
- if symptoms resolve in less than 24 hours

STROKE
NEUROLOGICAL DISORDERS
Initial treatment for Ischemia:
1. Oxygen – ABGs, Pulse oximetry
2. Glucose – serials checks of blood glucose levels, insulin sliding scale regimen or continuous
insulin infusion
3. Reperfusion (adequate blood flow) – IV t-PA or thrombolytic medications

Thrombolytic Drugs
IV t-PA (streptokinase) – dissolves the clot and permits reperfusion of brain tissue
- should be initiated as quickly as possible; 4.5 hours or less from the onset of neuro symptoms
- activates plasminogen

Anticoagulation
- dipyredamole, ticlopidine, clopidogrel (Plavix), aspirin (ASA)
- moderate consumption of leafy green vegetables containing vitamin K
- monitor prothrombin time and INR (bleeding); wof signs of bleeding
STROKE
NEUROLOGICAL DISORDERS
Control of Hypertension and Increased Intracranial Pressure
HTN – Diastolic BP 105 mmHg – lowered gradually
ICP elevations – short-term hyperventilation, fluid restriction, head elevation,
avoidance of neck flexion or severe head rotation, use of osmotic diuretics
(mannitol) to decrease cerebral edema

Surgical Management
Carotid endarterectomy to prevent stroke
Hemicraniectomy
Extracranial-intracranial bypass surgery

Nonsurgical Management
Carotid artery stenting
STROKE
NEUROLOGICAL DISORDERS
Emotional and Behavioral Modification
- controlling stimuli in the environment, providing rest periods, giving positive feedback,
providing repetition, reduce stress

Communication
Expressive or nonfluent dysphasia – patient understands language but is unable to use it
appropriately; Left Broca’s area (memory of motor patterns of speech is affected)
Receptive or fluent dysphasia – patient is unable to understand the meaning of the
spoken word (and usually the written word); left Wernicke’s area (control center for
recognition of spoken language)
Global dysphasia – both expressive and receptive dysphasia

STROKE
NEUROLOGICAL DISORDERS
SEIZURES is an episode of abnormal and excessive discharge of cerebral neurons
- it can result in altered sensory, motor or behavioral activities
- can be associated with changes in the LOC
- common sites are the frontal and temporal lobes, particularly the hippocampus in the medial
temporal lobe

EPILEPSY is a condition in which seizures are spontaneous and recurrent

STATUS EPILEPTICUS – a condition of either continued seizure activity or repetitive seizures over
a period of 30 minutes

Etiology:
Idiopathic – 50%,occur most often in children younger than 10 years of age Congenital and
Genetic causes – 10%
Causes: vascular disease, alcohol, cerebral tumors, trauma, infection or fever, metabolic
disturbances, anoxia, and degenerative diseases
SEIZURES
NEUROLOGICAL DISORDERS
Classification of Seizure types:

1. Generalized: involves both hemispheres; LOC; no local onset in the cerebrum

a. Tonic-Clonic (Grand Mal) – LOC; stiffening; forced expiration (cry); rhythmic jerking
b. Clonic – symmetrical, bilateral semirhythmic jerking
c. Tonic – sudden increased tone and forced expiration
d. Myoclonic – sudden, brief body jerks
e. Atonic (“drop attacks”) – sudden loss of tone, falls
f. Absence (petit mal) – brief staring, usually without motor involvement

2. Partial: involves one hemisphere

a. Simple partial seizure – no change in LOC, Jacksonian
b. Complex partial seizure – altered LOC;with or without automatisms; lip smacking,
swallowing, aimless walking, verbalizations
c. Partial with secondary generalization

SEIZURES
NEUROLOGICAL DISORDERS
Diagnostic Tests:
EEG, MRI, CT Scan
Epilepsy monitoring unit

DRUG THERAPY:
Carbamazepine (Tegretol)
Gabapentin (Neurontin)
Levitiracetam (Keppra)
Phenobarbital – potential CNS toxicity; taper slowly
Phenytoin (Dilantin) – dose guided by blood levels (10-20 mcg/ml); less expensive
- parenteral DILANTIN should be diluted in normal saline
Valproate (Depakote)

SEIZURES
NEUROLOGICAL DISORDERS
The symptoms of a Dilantin overdose vary. They may include:
Coma
Confusion
Fever
Involuntary, jerky, repeated movement of the eyeballs
(nystagmus)
Lethargy
Low blood pressure
Nausea and vomiting
Sleepiness
Slow or slurred speech
Staggering gait or walk
Swollen gums
Seizures
Tremor (uncontrollable, repeated shaking of the arms or legs)
Unsteadiness, uncoordinated movements
Guillain-Barre Syndrome
- also known as acute inflammatory demyelinating polyneuropathy
- is a rapidly evolving illness
- commonly presents as symmetrical weakness, sensory loss and areflexia
- is an inflammatory peripheral neuropathy in which lymphocytes and macrophages
strip myelin from axons
- it a referred as a syndrome, because of the combination of signs and symptoms

Etiology:
- half of patients have a mild febrile illness 2-3 weeks before the onset of symptoms
- respiratory or GI
- Campylobacter jejuni and cytomegalovirus are the causes of the most frequent
antecedent infections
GUILLAIN-BARRE SYNDROME (GBS)
NEUROLOGICAL DISORDERS
Clinical Manifestations:
- flaccid, ascending paralysis develops quickly
- commonly affected in a symmetrical pattern
- starts as a weakness in the lower extremities
- may develop rapidly over the course of hours to days
- 3-4 weeks to develop

Acute stage: onset of symptoms and rapidly progresses until no additional deterioration
Plateau stage: symptomatic, days to weeks
Recovery Phase: can take up to 2 years; remyelination and axonal degeneration;
remyelination 1-2 mm/day

GUILLAIN-BARRE SYNDROME (GBS)

NEUROLOGICAL DISORDERS
Clinical Management:

ICU admission
Mechanical Ventilation
Preventive measures- PE, DVT (heparin)
Intravenous immunoglobulin (IVIG) – adverse effect is acute tubular necrosis
Plasmapheresis – hemorrhage and catheter-related infections

Patient Education and Discharge Planning

Rehabilitation – 2 years
Support groups – Gullain-Barre Syndrome International Foundation

GUILLAIN-BARRE SYNDROME (GBS)

NEUROLOGICAL DISORDERS
MYASTHENIA GRAVIS
- is an autoimmune disorder of the neuromuscular junction transmission
- presents with fatigue and muscle weakness in the ocular, bulbar, diaphragm or limb muscles
- derived from the Greek words for “muscle” and “weakness” whereas gravis means “grave” in
Latin
- because of the high mortality related to diaphragmatic muscle weakness, the disorder was called
“grave muscle weakness”

Pathophysiology:
- acethycholine binds to the AChR
Epidemiology:
seen more often in women than in men at a ratio of 3:2

Clinical Manifestations:
Ocular Myasthenia or Generalized Myasthenia

MYASTHENIA GRAVIS
NEUROLOGICAL DISORDERS
 Diagnosis:
Electromyography EMG - needle electrode is inserted in skeletal muscle; electrical activity
Blood is drawn for AChR antibodies
Tensilon Test (edrophonium) – 10 mg IV Tensilon is given over 1 minute
- a response is anticipated within 2-3 minutes
- Atropine should be readily available in the event of bradycardia

Clinical Management:
Long-term immunosuppression with corticosteroids
Mycophenolate mofetil (CellCept)
Azathioprine (Imuran) or cyclosporine
Cyclophosphamide (Cytoxan)
IVIG
Plasmapheresis
Thymectomy

MYASTHENIA GRAVIS
NEUROLOGICAL DISORDERS
 Diagnosis:
Electromyography EMG - needle electrode is inserted in skeletal muscle; electrical activity
Blood is drawn for AChR antibodies
Tensilon Test (edrophonium) – 10 mg IV Tensilon is given over 1 minute
- a response is anticipated within 2-3 minutes
- Atropine should be readily available in the event of bradycardia

Pharmacological Management:
Pyridostigmine (Mestinon) – liquid, 60 mg tablet, 180 mg time-span formula or IV neostigmine
Muscarinic s/e: diarrhea, abdominal cramping, increased salivation, blurred vision, bradycardia
increased perspiration
Nicotinic s/e: muscle twitching, weakness and fatigue

MYASTHENIA GRAVIS
NEUROLOGICAL DISORDERS
Myasthenic crisis vs. Cholinergic crisis
Myasthenic crisis - respiratory failure along with sudden exacerbation of weakness in
other muscle groups
- caused by lack of medication or lack of responsiveness at the
neuromuscular junction to cholinergic treatment

Cholinergic crisis – are muscarinic or nicotinic side effects; increased erspiration,

abdominal cramping and diarrhea
- too much medication

MYASTHENIA GRAVIS
NEUROLOGICAL DISORDERS
Patient Education and Discharge Planning

Medications: purpose, schedules, side effects

Medical ID and Card
S/S of crisis
Avoid crowds – movies or concerts
Support groups – Myasthenia Gravis Foundation

MYASTHENIA GRAVIS
NEUROLOGICAL DISORDERS
INOTROPES IV COMPUTATIONS