Neurological Dysfuntion

Increased (ICP) Intracranial Pressure

o

Increased

concentration

of

carbon

dioxide will cause VASODILATION à

 Intracranial pressure more than 15 mmHg  

Brunner= Normal intracranial pressure 10-20 mmHg Monro-Kellie hypothesis: because of limited space in the skull, an increase in any one skull component—brain tissue, blood, or CSF—will cause a change in the volume of the others

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Compensation to maintain a normal ICP of 10 to 20 mm Hg is normally accomplished by shifting or displacing CSF

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With disease or injury, ICP may increase

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Increased ICP decreases cerebral perfusion, causes ischemia, cell death, and (further) edema

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Brain tissues may shift through the dura and result in herniation

increased flowà increased ICP 

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Cerebral Edema o

Abnormal accumulation of fluid in the intracellular space, extracellular space or both.

o

Edema can occur in gray, white or interstitial matter.

Herniation •

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 Autoregulation: refers to the brain’s ability to

Cerebral response to increased ICP •

The brain can maintain a perfusion pressure if the systolic blood pressure is 50 mm Hg and the ICP is less than Hg

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Cushing’s response- is seen when cerebral blood flow decreases significantly. When ischemic → vasomotor center triggers an increase in arterial pressure in an effort to overcome the increased ICP

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Vasomotor center triggers rise in BP to increase ICP

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Sympathetic response is increased BP but the heart rate is SLOW

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Respiration becomes SLOW

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CCP (cerebral perfusion pressure) is closely linked to ICP

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CCP = MAP (mean arterial pressure) – ICP

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Normal CCP is 70 to 100

•

A CCP of less than 50 results in permanent neuralgic damage

change the diameter of blood vessels to maintain cerebral blood flow during alterations in the systemic blood pressure

 CO2 plays a role; decreased CO2 results in vasoconstriction, and increased CO2 results in vasodilatation

 Pathophysiology • The cranium only contains the brain substance, the CSF and the blood/blood vessels • MONRO-KELLIE hypothesis- an increase in any one of the components causes a change in the volume of the other • Any increase or alteration in these structures will cause increased ICP • Increased ICP from any cause decreases cerebral perfusion, stimulates further swelling(edema, and may shift brain tissue through openings in the rigid dura, resulting in hernation, a dire and a frequently fatal event Compensatory mechanisms:  1. Increased CSF absorption  2. Blood shunting  3. Decreased CSF production Decompensatory mechanisms:  1. Decreased cerebral perfusion  2. Decreased PO2 leading to brain hypoxia  3. Cerebral edema  4. Brain herniation 

Decreased cerebral blood flow o Increased ICP significantly reduce cerebral blood flow, resulting in ischemia and cell death

o

Vasomotor

reflexes

are



steady arterial to 150 40 mm

Manifestations of Increased ICP—Early o

Changes in level of consciousness

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Abnormal respiratory and vasomotor response

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Any change in condition

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Restlessness, confusion, increasing drowsiness, increased respiratory effort, and purposeless movements has neurologic significance

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Stuporous, reactive only to loud and painful stimuli (serious stage of brain circulation is probably taking place)

stimulated

initiallyà systemic pressure rises to maintain cerebral blood flow à slow bounding pulses and respiratory irregularities

Results from an excessive increase in ICP when the pressure builds up and the brain tissue presses down on the brain stem

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Pupillary changes and impaired ocular movements(Pupillary changes- fixed, slowed response)

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Weakness in one extremity or one side

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Headache: constant, increasing in intensity, or aggravated by movement or straining

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Vomiting

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Comatose and abnormal motor response in the form of decortication (abnormal flexion of the upper extremities and extension of the lower extremities), decerbration (extreme extension of the upper and lower extremities) of flaccidity

o Evaluate neurologic status as completely as possible o

Glasgow Coma Scale

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Pupil checks

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Assess selected cranial nerves

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Take frequent vital signs

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Assess intracranial pressure

o Nursing interventions: o Maintain patent airway

 1. Elevate the head of the bed 15-30 degrees- to promote venous drainage

Manifestations of Increased ICP—Late

 2. assists in administering o

Respiratory and vasomotor changes

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VS: increase in systolic blood pressure, widening of pulse pressure, and slowing of the heart rate; pulse may fluctuate rapidly from tachycardia to bradycardia and temperature increase 

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Projectile vomiting

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Hyperthermia

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Abnormal posturing

•Mannitolto produce negative fluid balance

•anticonvulsants-p prevent seizures

Brain stem herniation: results from an excessive increase in ICP in which the pressure builds in the cranial vault and the brain tissue presses down on the brain stem. Results in cessation of blood flow to the brain, leading to irreversible brain anoxia and brain death. Diabetes Insipidus: results decreased secretion of ADH

3. Administer prescribed medications- usually

•corticosteroid- to reduce edema

Complications

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Cushing’s triad: bradycardia, hypertension, and bradypnea

o

o

100% oxygen or controlled hyperventilation- to reduce the CO2 blood levelsàconstricts blood vesselsàreduces edema

of

s/symp: excessive urine output, decreased urine osmolality and serum hyperosmolality o SIADH: is the result of increased secretion of ADH. Pt. becomes vol. overloaded, urine output diminishes, and serum sodium concentration becomes dilute.

o Nursing Process—Assessment of the Patient With Increased Intracranial Pressure o Conduct frequent and ongoing neurologic assessment

to

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4. Reduce stimuli

environmental

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5. Avoid activities that can increase ICP like valsalva, coughing, shivering, and vigorous suctioning

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6. Keep head on a neutral position. ACOID- extreme flexion, valsalva

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7. monitor for secondary complications •Diabetes insipidus- output of >200 mL/hr •SIADH

 Medical Management: o Monitoring Intracranial Pressure and Cerebral Oxygenation:  Ventriculostomy: a fine-bore catheter is inserted into a lateral ventricle, preferably in the non dominant hemisphere of the brain. Use to drain blood from the ventricle. Continuous drainage of CSF under pressure control is an effective method of treating intracranial hypertension.  Subarachnoid screw or bolt: is a hollow device that is inserted through the skull

and dura mater into the cranial subarachnoid space. Attached to the pressure transducer and the output is recorded on an oscilloscope.  Epidural monitor: uses a pneumatic flow sensor and functions without electricity. Disadvantage: inability to withdraw CSF for analysis  Fiberoptic monitor: or transducer-tipped catheter is an alternative standard intraventricular, subarachnoid and subdural system. o Decreasing Cerebral Edema

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o Large artery thrombotic stroke: caused by artherosclerosic plaques in the large blood vessels of the brain. Thrombus formation and occlusion at site of the artherosclerosis result in ischemia and infarction.

o Small penetrating artery thrombotic stroke: also called lacunar stroke because of the cavity that is created after the death of the infracted brain tissue o Cardiogenic embolic stroke: associated with cardiac dysrhythmias, usually atrial fibrillation. Embolic stroke can also be associated with valvular heart dse and thrombi in the left ventricle.

 Osmotic diuretics: such as mannitol may be administered to dehydrate the brain tissue and reduce cerebral edema. Act by drawing water across intact membranes, thereby reducing the volume of the brain and extracellular fluid.  If brain tumor is the caused of the increased ICP, corticosteroids (dexamethasone) help reduce the edema surrounding the tumor.  Limiting overall fluid intake leads to dehydration and hemoconcentration, which draws fluid across the osmotic gradient and decreases cerebral edema.  Lowering body temperature would decrease cerebral edema by reducing the oxygen and metabolic requirements of the brain, thus protecting the brain from continued ischemia. o Maintaining Cerebral Perfusion

o Cryptogenic stoke: which have no cause o Strokes from other causes: illicit drug use, coagulopathie, migraine and spontaneous dissection of the carotid or vertebral artery.

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obstruction of a blood vessel → initiates a complex series of cellular metabolic events referred to as the ischemic cascade → Cerebral blood flow decreases to less than 25 mL per 100g per minute → neurons are no longer maintain aerobic respirations → mitochondria switch to anaerobic which generates large amount of lactic acid, causing a change in the pH level → Neurons incapable of producing sufficient quantities of ATP → the membrane pumps electrolyte balance begin to fail and the cell cease to function.

volume and inotropic agents such as dobutamine hydrochloride (Dobutrex) and norepinephrine bitartate (Levophed). The effectiveness of the cardiac output is reflected in the CCP, which is maintained at greater than 70 mm Hg. Reducing Cerebrospinal Fluid and Intracranial Blood Volume  CSF drainage is frequently performed, because the removal of CSF with a ventriculostomy drain can dramatically reduce the ICP and restore CCP. Controlling Fever Fever increases cerebral metabolism and the rate at which cerebral edema forms.  Administration of antipyretic medications and use of hypothermia blanket Maintaining Oxygenation Reducing Metabolic Demands

o Early in the cascade an area of low cerebral blood flow, referred to as the penumbra region, exist around the area of infarction. The penumbra region is a ischemic brain tissue that may salvaged with timely intervention.

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o o

 Cellular metabolic demands may be reduced through the administration of high doses of barbiturates if the pt. is unresponsive to conventional tx. Barbiturates decrease ICP and protect the brain is uncertain; administration of pharmacologic paralyzing agents such as propofol (Diprivan) Cerebrovascular Accident/ ischemic stroke/ brain attack 

Sudden loss of function resulting from disruption of the blood supply to a part of the brain.

Pathophysiology

o Disruption of the cerebral blood flow due to

 Cardiac output is made using fluid

o

Different types of stroke based on the caused

o The penumbra area maybe revitalized by administration of tissue plasminogen activator.

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Clinical Manifestations o Numbness or weakness of the face, arm, or leg, especially on one side of the body o Confusion or change in mental status o Trouble speaking or understanding speech o Visual disturbances o Difficulty walking, dizziness, balance or coordination o Sudden severe headache

or

loss

of

o Homonymous hemianopsia: (loss of the half of the visual field); unaware of persons or objects on the side of visual loss, neglect of one side of the body; difficulty in judging distances.

 Motor loss o A stroke is an upper motor lesion and results in loss of voluntary control over motor movements.

 Nsg Intervention: place obj w/in intact field of vision, instruct/ remind pt. to turn head in the direction of visual loss to compensate for loss of visual field.

o Hemiplegia: paralysis of the face, arm, and leg on the same side ( due to the lesion on the opposite hemisphere) 

o Loss of peripheral vision: difficulty at seeing at night, unaware of objects or the borders of objects

Nsg Intervention: R.O.M., maintain body alignment, exercise unaffected limb to increase mobility, strength and use.

 Nsg Intervention: place obj at the center intact visual filed, encourage the use of crane or other objects to identify objects in the periphery of visual field

o Hemiparesis: weakness of the face, arm, and leg on the same side ( due to the lesion of the opposite side) 

o Diplopia: double vision

Nsg Intervention: provide object w/in the pt. reach on the non affected side, instruct the pt. to increase strength on unaffected side.

 Nsg Intervention: explain the location of object when placing it near the pt., consistently place pt. care items in same location

o Ataxia: staggering, unsteady gait; unable to keep feet together; needs a broad base to stand  

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Nsg Intervention: support pt. during the initial ambulation phase.

Communication Loss o Dysarthria: difficulty in forming words 

Nsg intervention: provide pt. w/ alternative method of communication, allow sufficient to verbal response

o Dysphagia: difficulty in swallowing 

Nsg Intervention: test the pt. pharyngeal reflexes before offering food or fluid, place food on the unaffected side of the mouth.

o Aphasia: loss of speech, could be expressive aphasia, receptive aphasia, or global (mixed) aphasia 

Expressive aphasia: unable to form words that are understandable; may be able to speak in single word responses (repeat sounds of the alphabet)

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Receptive aphasia: unable to comprehend the spoken words; can speak but may not make sense (speak slowly and clearly)

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Global (mixed) aphasia: combination of both receptive and expressive aphasia (speak clearly and in simple sentences, use gestures and pictures when able)

o Apraxia: inability to performed previously learned action

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Visual field deficits

Sensory Disturbances o Paresthesia: numbness or tingling of the extremities, difficulty with proprioception ( occurs on the side opposite the lesion)  Nsg Intervention: ROM, corrective devices as needed

apply

o Agnosias: deficit in the ability to recognize previously familiar objects perceived by one or more of the senses.  Assessment and Diagnostic Findings o Initial assessment: airway patency (may be compromised by loss of gag reflexes and altered respiratory pattern), cardiovascular status (including BP, cardiac rhythm and rate, carotid bruit) and gross neurologic deficits. o A transient ischemic attack (TIA) is a neurologic deficit lasting less than 24 hours, w/ most episodes resolving in less than 1 hr.

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Manifested by: sudden loss of motor, sensory, or visual function. (symp. Results from temporary ischemia to a specific region of the brain.) a TIA may serve as a warning sign of impending stroke. o Noncontrast CT scan: to determine if the event is ischemic or hemorrhagic o 12-lead electrocardiogram (ECG) and carotid ultrasound are standard test.  Prevention o Non-modifiable risk factors  Advanced age (people older than 55 yrs of age)  Gender (men have a higher rate of stroke than women)  Race (African-American) o Modifiable risk factors    

Hypertension Atrial fibrillation Hyperlipidemia Obesity

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o May result in an abrasion (brush wound), contusions, lacerations or hematoma beneath the layer of the tissue o Large-avulsion (tearing away) of the scalp could be life threatening o Diagnosis of scalp injury is based on P.E., inspection and palpation. o Area is irrigated b4 the laceration is sutured, to remove foreign material and to reduce the risk of infection. o Subgaleal hematomas (hematoma below the outer covering of the skull) usually absorb on their own and do not require any specific treatment.  Skull Fracture o Skull fracture: is break in the continuity of the skull caused by forceful trauma. o May occur w/ or w/out damage of the brain o Classification

Smoking Diabetes

 Medical Management o Artrial fibrillation (cardioembolic strokes) are treated w/ dose-adjusted warfarin sodium (Coumadin) international normalized ratio: 2.5 (if contraindicated can use aspirin) o Platelet inhibiting medications; aspirin, extended-release dipyridamole (Persantine) plus aspirin, clopidogrel (Plavix), and ticlopidine (Ticlid); decrease the incidence of cerebral infarction in pts. who experienced TIA and stroke from suspected embolic and thrombotic causes. o 3-hydroxy-2-methyl-glutaryl-coenzyme A reductase inhibitors (also known as statins) have been found to reduce coronary events and strokes; independent of cholesterol levels, and widely use for stroke prevention. o Thrombolytic Therapy:

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Dissolving the blood cloth that is blocking blood flow to the brain. Recombinant t-Pa is a genetically engineered form of t-Pa, a thrombolytic substance made naturally by the body. Binding to fibrin and converting plaminogen to plasmin, w/c stimulates fibrinolysis of the atherosclerotic lesion.

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Head Injuries  Head injury is a broad classification of that includes injury of the scalp, skull, or brain. Pathophysiology o Brain damage occurs at the moment of impact o Traumatic injury takes 2 forms:

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Primary Injury: initial damage to the brain that results from traumatic event. (Contusions, lacerations and torn blood vessel due to impact, acceleration/deceleration, or foreign object penetration.  Secondary Injury: evolves over the ensuing hours and days after the initial injury and is due primarily due to unchecked cerebral edema, ischemia and chemical changes associated with direct trauma to the brain.

o Bleeding or swelling w/in the skull→ increase the volume of contents → increases intracranial pressure → displacement of the brain through or against the rigid structures of the skull → restriction of blood flow to the brain→ decreasing oxygen and waste removal→ brain become anoxic and cannot metabolize properly producing ischemia, infarction, irreversible brain damage, and eventually, brain death. o Brain suffers from traumatic injury → brain swelling or bleeding; increases intracranial vol. → rigid cranium allow no room for expansion of contents so intracranial pressure increases → pressure on blood vessels w/in the brain causes blood flow to the brain to slow→ cerebral hypoxia and ischemia occur → Intracranial pressure continues to rise. Brain may herniate. → cerebral flow ceases

 Scalp Injury: minor injury

o

 Simple (linear) fracture is a break in the continuity of the bone.  A comminuted skull fracture refers to a splintered or multiple fracture line.  A fracture of the base of the skull is called a basilar skull fracture. A fracture may be open, indicating a scalp laceration or tear in the dura or closed, in w/c case the dura is intact. Clinical Manifestations o Persistent localized pain usually suggest that a fracture is present o Hemorrhage from the nose, pharynx or ears and blood may appear under the conjunctiva o Area a ecchymosis (bruising) may be seen over the mastoid (battle’s sign) o Basilar skull fractures are suspected when CSF escapes from the ear (CSF otorrhea) and nose (CSF rhinorrhea) o A halo sign (blood stain surrounded by a yellowish stain) may be seen in linens or in the head dressings and is highly suggestive CSF leak. Assessment and Diagnostic Findings o Radiologic Exam confirms the presence and extent of a skull fracture. o CT scan: uses high speed x-ray scanning to detect less apparent abnormalities. Fast, accurate, and safe diagnostic procedure that shows the presence, nature, location, and extent of acute lesion. o MRI: used to evaluate pts. w/ head injury when a more accurate picture of the anatomic nature of the injury is warranted and when the pt. is stable enough to undergo this longer procedure.  Medical Management o Depressed skull fractures usually require surgery. o B4 the surgery: the scalp is shaved and cleansed with copious amounts of saline to remove debris. o Fracture is exposed, skull fragments are elevated, any underlying dural laceration is repaired and any accompanying hematoma is evacuated. o Penetrating wounds require surgical debridement to remove foreign bodies and devitalized brain tissue and to control hemorrhage

o IV antibiotic is instituted immediately o CSF leakage: nasopharynx and external ear should be kept clean. (Usually piece of sterile cotton is placed loosely in the ear, or a sterile cotton pad may be tapped loosely under the nose or against the ear to collect the draining fluid.) o Head is elevated 30 degrees to reduce ICP and promote spontaneous closure of the leak Brain Injury o Brain injury: injury to the brain that is severe enough to interfere w/ normal functioning. o Closed (blunt) brain Injury occurs when the head accelerates and then rapidly decelerates or collides w/ another object (eg. Wall) and brain tissue is damaged but there is no opening through the skull and dura. o Open brain injury occurs when an object penetrates the skull, enters the brain, and damages the soft brain tissue in its path or when blunt trauma to the head is so severe that it opens scalp, skull, and dura to expose the brain. o Types of Brain Injury

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Concussion: temporary loss of neurologic function w/ no apparent structural damage. A concussion also referred as mild traumatic brain injury generally involves a period of unconsciousness lasting from a few seconds to a few minutes. * Only cause dizziness and spots in eyes (“seeing stars”) or it may be severe enough to cause loss of consciousness for a time * If frontal lobe is affected, pt. exhibit irrational behavior; temporal lobe produce temporary amnesia or disorientation. * Treatment involves observing the pt. for headache, dizziness, lethargy, irritability and anxiety. * Postconcussion Syndrome * Pt family is instructed to observed the ff. s/sym -Difficulty in awakening -Difficulty in speaking -Confusion -severe headache -Vomiting -weakness of one side of the body  Contusion: the brain is bruised, w/ possible surface hemorrhage. Pt. is unconscious for more than few second or minutes. * Pt. may lie motionless w/ faint pulse, shallow respirations, and cool pale skin. * Often involuntary evacuation of bowels and bladder occurs. * May be aroused w/ effort but soon slips back to unconsciousness. * BP and Temp are subnormal; similar to shock  Diffuse Axonal Injury: involves widespread damage to axons in the cerebral hemisphere, corpus callosum and brain stem. Can be mild, moderate or severe. * Pt. experiences no lucid intervals, immediate coma, decorticate, and decerebrate posturing.  Intracranial Hemorrhage: hematoma maybe epidural (above the dura), subdural

(below the dura) or intracerebral (w/in the brain). Major symptoms are delayed until the hematoma is large enough to cause distortion of the brain and increase ICP. * Epidural Hematoma (Extradural Hematoma or Hemorrhage) can result from a skull fracture that causes a rupture or laceration of the middle meningeal artery, the artery that runs between the dura and the skull inferior to a thin portion of temporal bone. And usually a momentary loss of consciousness followed by interval of apparent recovery (lucid interval).→ compensation for the expanding hematoma takes place by rapid absorption of CSF and decreased intravascular volume, both of w/c help maintain normal ICP. But if mechanism no longer compensates sign of compression appear (deterioration of consciousness & signs of focal neurologic deficits, such as dilation & fixation of pupil or paralysis of an extremity). Tx: making opening to the skull (burr holes), ↓ICP, remove cloth & control bleeding. Craniotomy and drain may be recquired. * Subdural hematoma collection of blood between the dura and the brain, a space normally occupied by a thin cushion fluid. It can also occur as a result of coagulopathies or rupture of an aneurysm. Venous in origin and is caused by the rupture of small vessels that bridge the subdural space. Acute Subdural Hematoma asso. w/ major injury (contusion & laceration). Clinical Manifestations develop over 24 to 48 hrs. S/Sym includes changes in LOC, pupillary sign and hemiparesis. Subacute Subdural Hematoma result of less severe contusion and head trauma. Clinical manifestations appear 48 hrs. to 2 weeks. Chronic Subdural Hematoma it is seemly minor head injury and most common to elderly. Elderly are prone to this injury secondary to brain atrophy, w/c is frequent consequence of the aging process. The time of the injury and onset of symptoms can be lengthy. It may be mistaken to stroke. Bleeding is less profuse but compression of the intracranial contents still occurs. The blood w/in the brain changes in character in 2 to 4 days, becoming thicker and darker. Cloth breaks down and has the color and consistency of motor oil. Symptoms include severe headache (come & go), alternating focal neurologic sign, personality changes; mental deterioration & focal seizures. * Intracerebral Hemorrhage & Hematoma is commonly seen in head injuries when force is exerted to the head over a small area. Its onset may be insidious, begin w/ the development of neurologic deficits ff by headache. Management includes supportive care, control of ICP, and careful administration of fluids and electrolytes and hypertensive medications.  Medical Management

o CT and MRI scans are the primarily neuroimaging diagnostic tools are useful in evaluating the brain structure. o Pt. is transported on a board w/ the head and neck maintained in alignment w/ the axis of the body. o A collar spine should be applied until cervical spine x-ray have been obtained and recorded.  Brain Death o 3 cardinal signs of brain death: coma, absence of brain stem reflexes and apnea. o Adjunctive test such as ECG and cerebral blood flow (CBF) studies are often use to confirm brain death. Spinal Cord Injury  Pathophysiology o Transient concussion (from w/c the pt. full recovers) to contusion o Laceration and compression of the cord substance (either alone or combination) o Complete transaction (severing) of the cord (w/c renders the pt. paralyzed below the level of injury) o Primary Injuries: Result of the initial assault or trauma and usually permanent. o Secondary Injuries: usually the result of a contusion or tear injury, in w/c the nerve fibers begin to swell and disintegrate. o A secondary chain event produces ischemia, hypoxia, edema and hemorrhagic lesion, w/c in turn result in destruction of myelin and axons.  Clinical Manifestations o Incomplete Spinal cord lesions (the sensory or motor fibers or both are preserved below the lesion. o “Neurologic Level” refers to the lowest level at w/c sensory and motor functions are normal. Below the neurologic level, there is total sensory and motor paralysis, loss of bladder and bowel control (usually w/ urinary retention and bladder distention), loss of sweating and vasomotor tone, and marked reduction of BP from loss of peripheral vascular resistance. o Complete Spinal cord lesion: (total loss of sensation and voluntary muscle control below the lesion) can result in paraplegia (paralysis of the lower body) or tetraplegia (formerly quadriplegia- paralysis of all 4 extremities). o If conscious the client complains acute pain in the back or neck, w/c radiates along the involve nerve. Injury level

C1

C2 to C3

Segmenta l Sensorimo tor Function Little of no sensation or control of head and neck, no diaphragm control; requires continuous ventilation. Head and neck sensation; some neck

Dressing, eating

Eliminatio n

Mobility*

Dependent

Dependent

Limited. Voice or sip-n-puff controlled electric wheel chair

C4

C5

C6

C7 to C8

T1 to T5

T6 to T10

T11 to L5

S1 to S5

Dependent

Dependent

Same as C1

Dependent, may be able to eat w/ adaptive sling

Dependent

Limited to voice, mouth, head, chin, or shouldercontrolled electric wheel chair

Independen t w/ assistance

Maximal assistance

Independen t or w/ minimal assistance

Independen t or w/ minimal assistance

Electric or modified manual wheel chair, need transfer assistance Independen t in transfers and wheelchair

Independen t

Independen t

Independen t, manual wheel chair

Independen t

Independen t

Independen t, manual wheel chair

Independen t

Independen t

Independen t, manual wheel chair

Independen t

Independen t

Short distance to full ambulation w/ assistance

Independen t

Normal to impaired bowel and bladder function

Ambulate independen tly w/ or w/out assistance.

Assessment and Diagnostic Findings o Diagnostic X-ray (lateral cervical spine x-ray) & CT scan o MRI scan: if ligamentous injury is suspected Emergency Management o Pt. must be immobilized on spinal (back) board, w/ head & neck in neural position o One member of the team must assume control on the pts. head to prevent flexion, rotation or extension; done by placing the hands on both sides of the pts. head at about 

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control; independen t of mechanical ventilation for short periods. Good head and neck sensation and motor control; some shoulder elevation; diaphragm movement Full head and neck control; shoulder strength; elbow flexion Full innervated shoulder, wrist extension or dorsiflexion Fell elbow extension; some finger control Full hand finger control; use of intercostals & thoracic muscle Abdominal muscle control, partial to good balance w/ trunk muscles Hip flexors, hip abductor (L1-L3); knee extension (L2-L4), knee flexion and ankle dorsiflexion (L4-L5) Full leg, foot, and ankle control, innervation s of perineal muscles for bowel, bladder and sexual function (S2-S4)

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ear level to limit movement and maintain alignment while the spinal board or cervical immobilizing device is applied. Effects of Spinal Cord injuries o Central Cord Syndrome 

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Charac: motor deficit (in the upper extremities compared to the lower extremities; sensory loss variesbut is more pronounced in the upper extremities), bowel and bladder dysfunction is variable, or function maybe completely preserved. Cause: injury or edema of the central cord, usually of the cervical area. May be caused by hypertension injuries.

Anterior Cord Syndrome Charac: Loss of pain, temp, & motor function is noted below the level of the lesion; light touch, position, & vibration sensation remain intact.  Cause: The syndrome may be caused by acute disk hernation of hyperflexion injuries associated w/ fracture dislocation of vertebra. Ti may also occur as a result of injury to the anterior spinal artery, w/c supplies the anterior two thirds of the spinal cord. Brown-Séquard syndrome (Lateral cord Syndrome)  Charac: Ipsilateral paralysis or paresis is noted, together w/ ipsilateral loss of touch, pressure, & vibration & contralateral loss of pain and temp.  Cause: the lesion is caused by a transverse hemisection of the cord (half of the cord is transected from north to south), usually as a result of a knife and missile injury, fracture-dislocation of unilateral articular process, or possibly an acute ruptured disk. Medical Management o Pt. is resuscitated as necessary & oxygenation & cardiovascular stability are maintained. o Pharmacologic Therapy 

o

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High dose corticosteroids, specifically methylprednisolone found to improve motor and sensory outcomes Respiratory Therapy Oxygen is administer to maintained a high partial pressure of oxygen (Pa02), because hypoxemia can create or worsen a neurologic deficit of the spinal cord.  Diaphragmatic pacing (electrical stimulation of the pheric nerve) attempts to stimulate the diaphragm to help pt. breath. Skeletal Fracture Reduction & Traction 

o

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Gardner-Wells tongs require no predrilled holes in the skull. Crutchfield & Vinke tongs are inserted through holes made in the skull w/ a special drill under local anesthesia. Traction force is exerted along the longitudinal axis of the vertebral bodies, w/ the pt. neck in neural position. As the amount of traction is increased, the spaces between the intervertebral disks widen & the vertebrae are given a chance to slip back into position.

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A halo device may be used initially w/ traction, or may be applied after the removal of the tongs. It is consisting of a stainless-steel halo ring that is fixed to the skull by 4 pins. The pins are attached to a removable halo vest. It allows immobilization of the cervical spine while allowing early ambulation

 Spinal and Neurologic Shock o Spinal shock asso. w/ SCI reflects a sudden depression of reflex activity in the spinal cord (areflexia) below the level of injury. Below level of the lesion are w/out sensation, paralyzed, & flaccid and reflexes are absent. Bowel distention & paralytic ileus can be cause by depression of the reflexes & are treated w/ intestinal decompression by insertion of nasogastric tube. o A neurologic shock develops due to the loss autonomic nervous system function below the level of lesion. The vital organs are affected, causing BP and heart rate to ↓. This loss of sympathetic innervation → ↓ cardiac output, venous pooling in the extremities & peripheral vasodilatation.

 Deep Vein Thrombosis o Pt. who develop DVT are at risk for pulmonary embolism (pleuritic chest pain, anxiety, SOB, & abnormal blood gas values. ↑PaCO2 & ↓ PaO2) o The pt. should be assessed for a low grade fever, w/c is 1st sign of DVT, and thigh & calf measurement are made daily. o Low dose of anticoagulation therapy usually is iniated to prevent DVT & PE; thigh-high elastic compression stockings or pneumatic compression devices.  Other Complications o Respiratory complications o Autonomic dysreflexia: characterized by pounding headache, profuse sweating, nasal congestion, piloerection (“goose bumps”), bradycardia & hypertension. Altered Level of Consciousness  Not oriented, does not follow commands  Needs persistent stimuli to achieve a state of alertness  Loc is gauged on a continuum with a normal state of alertness and full cognition (consciousness) on the end and coma on the other.

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Coma is the clinical state of unarousable, unresponsive in which there is no purposeful response to internal or external stimuli, although nonpurposeful responses to painful stimuli & brain stem reflex may be present

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Akenitic Mutism a state of unresponsiveness to the environment in which the pt. makes no voluntary movement

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Persistent Vegetative state a condition in which the unresponsive pt. resume sleep-awake cycles after coma but is devoid of cognitive or affective mental function

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Locked-in-syndrome result from a lesion affecting the pons, & results in tetraplegia (quadtriplegia), inability to speak, but vertical eye movements and lid elevation remain intact and are used to indicate responsiveness.

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Pathophysiology

o Cause may be neurologic (head injury, stroke) toxicologic (drug dose, alcohol intoxication) or metabolic (hepatic or heparin failure, diabetic ketoacidosis) o Distruption of the cells of the nervous system, neurotransmitter or brain anatomy → faulty impulse transmission → impending communication with the brain or from the brain to other parts of the body. These disruptions are caused by cellular edema or other mechanism  Clinical Manifestations o Changes in pupillary responses, eye opening response, verbal response and motor response o Initial: subtle behavioral changes such as restlessness & ↑ anxiety o Pupils: sluggish, comatose: pupils become fixed; does not open the eyes  Assessment and Diagnostic findings o Evaluation of mental status, cranial nerve function, cerebellar function (balance & coordination), reflexes & motor & sensory function o Pt. is comatose but pupillary light reflexes are preserved, a toxic metabolic disorder is suspected o Start by assessing the verbal response o Determining the pt. orientation to time, person & place assess o Alertness is measured by the pt. ability to open eyes spontaneously or response to vocal or noxious stimulus (pressure or pain) o Motor response includes spontaneous, purposeful movement

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Complications o Respiratory distress/ failure o Pneumonia o Aspiration o Pressure ulcer o DVT o Contractures  Nursing Interventions o Maintaining airway 

Elevating the head of the bed to 30 degrees helps prevent aspiration

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Mouth is inspected for dryness, inflammation & crusting Unconscious pt. needs continuous oral care, bec risk of parotitis if the mouth is not kept scrupulously clean

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Cleansed & rinsed carefully to remove secretions & crusts & to keep the mucous membranes moist  A thin coating of petrolatum on the lips to prevent drying, cracking & encrustations  If w/ ET tube; tube should be moved to the opposite side of the mouth daily to prevent ulceration of the mouth and lips o Maintaining skin and joint integrity  

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Regular schedule of turning to avoid pressure Turning also provides kinesthetic (sensation of movement), proprioceptive (awareness of position) & vestibular (equilibrium) Maintaining correct body position is important Use of splints or foam boots aids in the prevention of foot drop & use of torachanter rolls to support the hip joints keep legs in proper alignment

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Arms are in abduction, finger lightly flexed and hands in slight supination o Preserving Corneal Integrity Eyes may be cleansed w/ cotton balls moistened w/ sterile normal saline to remove debris & discharge  Cold compress may be prescribed o Maintaining Body temperature 

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Slight elevation of temp may be caused by dehydration Removing all bedding over the pt. (w/ the possible exception of light sheet or small drape) Administering acetaminophen Giving cool sponge bath & allowing electric fan to blow over the pt. to increase surface cooling Use hypothermia blanket Temperature monitoring

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Positioning the pt. in lateral or semiprone position also helps, bec it permits the jaw & tongue to fall forward, thus promoting drainage of secretions  Suctioning is performed to remove secretions from the posterior pharynx and upper trachea  Chest physiotherapy & postural drainage may be initiated to promote pulmonary hygiene, unless contraindicated by the pts. underlying condition.  Chest should be auscultated at least every 8 hours to detect adventitious breath sounds or absence of breath sounds o Protecting the Patient Side rails are padded Providing privacy & speaking to pt. during nursing activities o Maintaining Fluid balance and Managing Nutritional Needs  

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IV solutions (blood transfusion) for pt. w/ ↑ ICP should be slowly o Proving Mouth Care

o Preventing Urinary Retention 

Bladder is palpated or scanned at intervals to determine whether urinary retention is present

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Pt. is not voiding, an indwelling urinary catheter is inserted & connected to a close drainage  A catheter may also be inserted during the acute phase of illness to monitor urinary output  Pt. is observed for fever & cloudy urine o Promoting Bowel Function

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Abdomen is assessed for distention by listening for bowel sounds & measuring the girth of the abdomen w/ tape measure Nurse monitors the number & consistency of bowel movements & performs a rectal examination for signs of fecal impaction Stool softeners may be prescribed To facilitate bladder emptying, a glycerin suppository may be indicated

Pt. may be require enema every other day to empty the lower colon o Providing sensory stimulation 

Nurse touches & talk to the pt. & encourages family members & friends to do so. Communication is extremely important & includes touching the pt. & spending enough time w/ the pt. to be become sensitive to his/ her needs  Nurse orients the pt. to time & place at least once every 8 hours  Minimize stimulation by limiting background noises, having one person to speak to pt. at a time, giving pt. a longer time to respond & allowing frequent rest or quiet times o Meeting the family needs o Monitoring & Managing potential complications

Atonic seizures Myoclonic seizures (bilaterally massive epileptic) Unclassified seizures

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Vital signs & respiratory function are monitored closely to detect any signs of respiratory failure or distress

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Chest physiotherapy & suctioning are initiated to prevent pneumonia LOC is monitored closely for evidence of impaired skin integrity & strategies to prevent skin breakdown & pressure ulcers Care is taken to prevent bacterial contamination of pressure ulcers, w/c may lead to sepsis or septic shock DVT: prophylaxis such as subcutaneous heparin or low molecular-wgt heaparin Thigh elastic compression sock

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Seizures  Episodes of abnormal motor, sensory, autonomic or psychic activity (or combination of these) that result from sudden excessive discharge from cerebral neurons

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Partial Seizures: begin in one part of the brain Partial seizure, consciousness remains intact; complex partial seizure consciousness is impaired Generalized Seizures: involve discharges in the whole brain

electrical

International Classification of Seizures PARTIAL SIEZURES (SEIZURES BEGINNING LOCALLY) Simple Partial Seizures (w/ elementary symptoms, generally w/out impairment of consciousness) • w/ motor symptoms • w/ special sensory or somatosensory symptoms • w/ autonomic symptoms • compound forms Complex Partial seizures (w/ complex symptoms, generally w/ impairment of consciousness) • w/ impairment of consciousness only • w/ cognitive symptoms • w/ affective symptoms • w/ psychosensory symptoms • w/ psychomotor symptoms (automatism) • Compound forms Partial seizure secondary generalized GENERALIZED SEIZURES (CONVULSIVE OR NON CONVULSIVE, BILATERALLY SYMMETRIC, W/OUT LOCAL ONSET) Tonic Clonic seizures Tonic seizures Clonic seizures Absence (petit mal) seizures

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Cause: Electrical disturbances (dysrhythmia) in the nerve cell in one section of the brain, these cells emit abnormal, recurring, uncontrolled electrical discharges. The characteristic seizure is a manifestation of excessive neural discharge. Asso. Loss of consciousness, excess movement or loss of muscle tone Can be idiopathic (genetic, developmental defects) Acquired seizure: o Cerebrovascular dse o Hypoxemia of any cause, including vascular insufficiency o Fever (childhood) o Head injury o Hypertension o CNS infection o Metabolic and toxic conditions (e.g. renal failure, hyponatremia, hypocalcemia, hypoglycemia, pesticides) o Brain tumor o Drug and alcohol w/drawal o Allergies

Nursing Management During Seizure • The circumstances b4 the seizure • The occurrence of the aura ( a premonitory or warning sensation that can be visual, auditory or olfactory) • Where the movement or the stiffness begins, conjugate gaze position and the position of the head at the beginning of the seizure (gives clues to the location of the seizure origin in the brain) • The type of movements in the part of the body involved • The areas of the body involved (turn back bedding to expose pt.) • The size of both pupils & whether the eyes are open • Whether the eyes or the head turn to ones side • The presence or absence of automatism (involuntary motor activity, such as lip smacking or swallowing) • Incontinence of urine and stool • Duration of each phase of the seizure • Unconsciousness • Any obvious paralysis or weakness of arms or legs after the seizure • Inability to speak after the seizure • Movements at the end of seizure • Whether or not the patient sleeps afterward • Cognitive status (confused or not confused) after the seizure • PREVENT INJURY

After a Seizure • The nurse role is to document the events leading to and occurring during and after the seizure • The pt. is at risk for hypoxia, vomiting & pulmonary aspiration • To prevent complication: pt. placed in side lying position to facilitate drainage of oral secretions & suctioning is performed

• Bed is placed on a low position w/ two or three side rails up and padded

Headache

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Head, or cephalgia, is one most common physical complain It may indicate organic dse (neurologic), a stress response, vasodilation (migraine), skeletal muscle tension(tension headache) Primary headache is one of which no organic cause can be identified. Types: migraine, tensiontype and cluster headaches. o Migraine is a symptom complex characterized by periodic and recurrent attacks of severe headache lasting from 4 to 72 hrs. in adults. It is primarily a vascular disturbance that occurs more commonly in women and has strong familial tendency o Tension type headache tend to be chronic and less severe and are probably the most common type of headache. o Cluster headaches are severe form of vascular headache, frequently in men. o Cranial arteritis is a cause of headache in the older population, reaching its incidence in those older than 70 yrs old. Inflammation of the cranial arteries is characterized by a severe headache localized at the region of temporal arteries.

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Secondary headache: is a symptom associated w/ an organic cause, such as brain tumor or an aneurysm. Assessment and Diagnostic Evaluation  Detailed history, a PA of head and neck and a complete neurologic examination  Headache may be a symptom of endocrine, hematologic, gastrointestinal, infectious, renal, cardiovascular or psychiatric dse.  Medication history: antihypertensive agents, diuretic medications, anti-inflammatory agents and monoamine oxidase (MOAI) inhibitor (few medications that provoke headache)  Sleep pattern, level of stress, recreational interests, appetite, recreational interest & family stressors are relevant  Questions include: o Location of headache, does it radiate? o Quality- dull, aching, steady, boring, burning, intermittent, continuous, paroxysmal o Precipitating factors o What makes head ache worse? o How long does a typical headache last o What relieves the headache? o Does nausea, vomiting, weakness or numbness in the extremities accompany the headache? o Insomnia, loss of appetite, loss of energy o Family history of headache 

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Neurologic examination, angiography, or MRI may underlying causes

CT, used

to

cerebral detect

Electromyography (EMG) may reveal a sustained contraction of the neck, scalp, or facial muscle. Pathophysiology  s/symp of migraine result from dysfunction of the brain stem pathways that normally modulate sensory input  Abnormal metabolism of serotonin, a vasoactive neurotransmitter found in the platelets & cells of

the brain, plays a major role. ( rise in plasma serotonin, w/c dilates cerebral vessel)  Migraine can be triggered by : menstrual cycle, bright lights, stress, depression, sleep deprivation, fatigue, overuse of certain medications & certain foods containing tyramine, monosodium glutamate, nitrites, or milk product & use of oral contraceptives.  Emotional or physical stress may cause contraction of the muscles of the neck & scalp resulting in tensiousterzn headaches.  Cluster headache: caused by dilation of orbital & nearby intracranial arteries  Cranial arteritis is thought to represent an immune vasculitis in w/c immune complexes are deposited w/in the walls of affected blood vessel, producing vascular injury & inflammation. Clinical Manifestations  Migraine: w/ aura can be divided into 4 phases:

• Prodrome: (60%) symptoms occur hrs. to day’s b4 a migraine headache. * Symp: depression, irritability, feeling cold, food cravings, anorexia, change in activity level, ↑ urination, diarrhea or constipation.

• Aura Phase: (31%); aura usually lasts less than 1 hr & may provide enough time for pt to take prescribed medication to avert a full-blown attack. * Period is characterized by focal neurologic symptoms, visual disturbances & may be hemianopic (affecting only half of the visual field. * Other symptoms may include numbness & tingling of the lips, face or hands; mild confusion; slight weakness of an extremity; drowsiness & dizziness * The period of an aura corresponds to the painless vasoconstriction that is the initial physiologic change characteristic of classic migraine * Cerebral blood flow studies are performed: during headache demonstrate that during all phases of the attack, cerebral blood flow is reduced throughout of the brain, w/ subsequent loss o autoregulation & impaired carbon dioxide responsiveness. • Headache Phase: as vasodilation & decline in serotonin levels occur, a throbbing headache intensifies over several hours * This headache is severe & incapacitating & is often associated w/ photophobia, nausea, & vomiting. Its duration varies, ranging from 4 to 72 hours. • Recovery Phase (termination or postdrome): the pain gradually subsides *Muscle contraction in the neck & scalp is common, w/ associated muscle ache & localized tenderness, exhaustion, & mood changes * Any physical exhaustion exaggerates the headache.  Tension-type headache: characterized by steady, constant feeling of pressure that usually begins in the forehead, temple, or back of the neck. * Band like or may be described as “a wgt. On top of my head”  Cluster headache: unilateral & come in cluster of one to eight daily, w/ excruciating pain localized to the eye & orbit & radiating to the facial & temporal regions. * The pain is accompanied by watering of the eye & nasal congestions.

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* Each attack min. to 3 hrs & may have a crescendo-decrescendo pattern. * Often described as “penetrating” Cranial arteritis: often begins w/ general manifestations such as fatigue, malaise, wgt loss & fever. * Manifestations include inflammation; sometimes a tender or swollen or nodular temporal artery is visible. * Visual problems are caused by ischemia over involved structure.

Prevention  Two beta-blocking agents propranolol (Inderal) & metoprolol (Lopressor) , inhibit the action of beta receptors- cells in the heart & brain that control the dilation of blood vessel Medical Management  Abortive approach, best employed in those pt. who have less frequent attacks, is aimed in relieving or limiting a headache at the onset or while in progress.  Preventive approach is used in pt. who experience more frequent attacks at regular or predictable intervals & may have a medical condition that precludes the use of abortive therapies.

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Triptans, serotonin receptor agonist, are the most specific antimigraine; these agent causes vasoconstriction, reduce inflammation, & may reduce pain transmission

• Triptan is Sumatriptan Succinate (Imitrex); available in oral, intranasal & subcutaneous preparations & is effective for the treatment of acute migraine & cluster headaches in adults. Effective in relieving moderate to severe migraine headaches in large number of adult pt. Sumatriptan can cause chest pain & is contraindicated for pt’s. w/ ischemis heart dse.

• Tiptans should not be taken w/ medications 

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containing ergotamine, because of potential prolonged vasoactive reaction. Ergotamine tartrate acts on smooth muscle, causing prolonged constriction of cranial blood vessels. Side effects include aching muscles, paresthesias (numbness & tingling), N/V. Cafergot, a combination of ergotamine & caffeine, can arrest or reduce the severity of the headache if it is taken at the first sign of an attack.

Classified into aseptic & septic meningitis. o Septic meningitis is caused by bacteria o Aseptic meningitis is caused by viral or secondary to lymphoma, leukemia or HIV. Pathophysiology  Origin: (1) through the blood stream as a consequence of other infections or (2) by direct spread, such as might occur after traumatic injury to the facial bones or secondary to invasive procedures  N. meningitis concentrates in the nasopharynx & is transmitted by secretion or aerosol contamination. 

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Causative organism enters the bloodstream→ it crosses the blood-brain barrier & proliferates in the CSF → host immune response stimulates the release of cell wall fragments & lipopolysaccharides, facilitating inflammation of the subarachnoid & pia mater → increased ICP  CSF circulates through the subarachnoid space, where inflammatory cellular materials from the affected meningeal tissue enter & accumulate. CSF studies demonstrate ↓ glucose, ↑ protein levels, & ↑ WBC count Clinical Manifestations

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(+) Brudzinski’s sign: when the pt. neck is flexed (after ruling out cervical trauma or injury), flexion of the knees & hips is produced; when the lower extremity of one side is passively flexed, a similar movement is seen in the opposite extremity. More sensitive indication of meningeal irritation.

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Photophobia(extreme sensitivity to light) Rash can be striking feature of N. meningitis infection Skin lesions develop, ranging from a petechial rash w/ purpuric lesions to large areas of ecchymosis Disorientation & memory impairment

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For acute attack of cluster headache: 100% oxygen face mask for 15 minutes, ergotamine tartrate, sumatriptan, corticosteroids or a percutaneous sphenopalatine ganglion blockade.  Early administration of a corticosteroid to prevent the possibility of loss of vision due to vascular occlusion or rupture of the involved artery. Nursing Management  Provide comport measures such as quiet, dark environment  Elevation of the head of the bed to 30 degrees  Symptomatic treatment such as antiemetics may be indicated  Symptomatic pain relief for tension headache may be obtained by application of local heat or massage.  Use of analgesic, antidepressant medications & muscle relaxant. Meningitis

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Inflammation of the pia mater, the arachnoid & the CSF- filled subarachnoid space

Headache & fever are frequently the initial symptoms. Fever tends to remain high throughout the course; headache is usually either steady or throbbing & very sever as a result og menigeal irritation Nuchal rigidity (stiff neck): early sign. Any attempts as flexion of the head are difficult because of spasms in the muscle of the neck. Forceful flexion causes severe pain. (+) Kernig’s sign: when the pt. is lying w/ the thigh flexed on the abdomen, the leg cannot be completely extended

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Behavioral manifestations; as illness progress, lethargy, unresponsiveness & coma may develop.

Seizures in adults w/ S.pneumoniae meningitis & are the result of areas irritability in the brain → ICP ↑ secondary to the accumulation of purulent exudates (initial signs of ↑ ICP include: ↓ LOC & fucal motor deficits). If ICP is not controlled, the uncus of the temporal lobe may herniate through the tentorium, causing pressure on the brain stem.  Acute fulminant infection producing signs of overwhelming septicemia: an abrupt onset of high fever, extensive purpuric lesions (over the face & extremities), shock & signs of disseminated intravascular coagulopathy. Assessment and Diagnostic Findings  Bacterial culture & Gram staining of CSF & blood are key diagnostic test.  Presence of polysaccharide antigen in CSF further supports the diagnosis of bacterial meningitis.

Medical Management  Penicillin antibiotic (eg. Ampicillin, pipercillin)  Cephalosporins  Vancomycin hydrochloride alone or in combination w/ rifampin may be used if resistant strains of bacteria are identified.

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Dexamethasone has been shown to be beneficial as adjunct therapy in the treatment of acute bacterial meningitis & in pneumococcal meningitis if it is administered 15 to 20 minutes b4 the 1st dose of antibiotic & every 6 hours for the next 4 days. Nursing Management  Neurologic status & vital signs are continually assessed  Pulse oximetry & arterial blood gas values are used to quickly indentify the need for respiratory support in ↑ ICP compromises the brain stem

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Insertion of a cuffed endotracheal tube & mechanical ventilation may be necessary to maintain adequate tissue oxygenation.  Arterial blood pressure are monitored to assess incipient shock  Measures are taken to reduce body temperature as quickly as possible. (Fever also increases the workload of the heart & cerebral metabolism. ICP will increase in response to the increased cerebral metabolic demands)  Protecting the pt. form injury secondary to seizure activity or altered LOC  Monitoring body wgt daily  Preventing complications associated w/ immobility such as pressure ulcers & pneumonia BRAIN ABSCESS Pathophysiology  Brain abscess is a collection of infectious material w/in the tissue of the brain  Most common predisposing conditions for abscess among immunocompetent adults w/ otitis media & sinusitis  An abscess can result form intracranial surgery, penetrating head injury, or tongue piercing

antimicrobial therapy directed at the abscess & the primary source of infection.  Corticosteroids may be prescribed to help reduce the inflammatory cerebral edema if the pt shows evidence of an increasing neurologic deficit. Nursing Management  Continuing to assess the neurologic status, administering medications, assessing the response to treatment and providing supportive care.  Ongoing neurologic assessment alerts the nurse to changes in ICP  The nurse also assesses and documents the responses to medications  Administration of insulin or electrolyte replacement may be required to return these values to normal or acceptable levels.

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MULTIPLE SCLEROSIS  Multiple sclerosis (MS) is an immune-mediated, progressive demyelinating dse of the CNS.  Demyelination refers to the destruction of myelin, the fatty & protein material that surrounds certain nerve fibers in the brain & spinal cord; it result in impaired transmission of nerve impulses.  Genetic predisposition is indicated by the presence of a specific cluster (haplotype) of human leukocyte antigens (HLA) on the cell wall. Presence of this haplotype may promote susceptibility to factors, such as viruses, that trigger the autoimmune response activated in MS.  DNA on the viruses mimics the amino acid sequence of myelin, resulting in an immune system cross-section in the presence of a defective immune system. Pathophysiology  Sensitized T cells typically cross the blood-brain barrier: their function is to check the CNS for antigens & then leave.

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Organism causing brain abscess may reach the brain by hematologic spread from the lungs, gums, tongue or heart or from a wound or intraabdominal infection  To prevent brain abscess, otitis media, mastoiditis, sinusitis, dental infections & systemic infections should be treated promptly. Clinical Manifestations  Manifestations result form alterations in intracranial dynamics (edema, brain shift), infection, or the location of the abscess.  Headache, usually worse in the morning, is the most prevailing symptoms.  Fever, vomiting, & focal neurologic deficits occurs as well.  Focal deficits such as weakness & decreasing vision reflect the area of brain that is involved.

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As abscess expands symp. Of increase ICP such as decreasing LOC & seizures are observed. Assessment and Diagnostic Findings

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Neurologic studies such as MRI and CT identify the size & location of the abscess.  Aspiration of the abscess, guided by CT or MRI is the best method to culture & identify the infectious organism. Medical Management  Treatment is aimed at controlling the increased ICP, draining the abscess & providing

Pt. safety is another key nursing responsibility.

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Sensitized T cells remain in the CNS & promote filtration of other agents that damage the immune system → immune system attack leads to inflammation that destroys myelin (w/c normally insulates the axon & speeds the conduction of impulses along the axon.) → the oligodendroglial cells that produce myelin in the CNS.

Demyelination interrupts the flow of nerve impulses & results in variety of manifestations.  Plaques appear on demyelinated axons, further interrupting the transmission of impulses. Demyelinated axons are scattered irregularly throughout the CNS.  Areas most frequently affected are the optic nerves, chiasm, and tracts; the cerebrum; the brain stem & cerebellum; and spinal cord.  Eventually, the axons themselves begin to degenerate, resulting in permanent & irreversible damage. Clinical Manifestations  Benign course & symptoms are so mild that the pt. does not seek health care or treatment  Primary progressive MS may result in quadriparesis, cognitive dysfunction, visual loss & brain stem syndromes.  Primary symptoms: fatigue, depression, weakness, numbness, difficulty in coordination, loss of balance, & pain.  Visual disturbances due to lesions in the optic nerves or their connections may include blurring

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of vision, diplopia (double vision), patchy blindness (scotoma) and total blindness. Fatigue is defined as a subjective lack of physical or mental energy that interferes w/ desired activity. Depression, heat, anemia, deconditioning & medication may contribute to fatigue. Avoiding heat temperatures, effective treatment of depression & anemia, and physical therapy my control fatigue. Lesions on the sensory pathways cause pain. Additional sensory manifestations: paresthesias, dysesthesias & propprioception loss. Spasticity (muscle hypertonicity) of the extremities and loss of the abdominal reflexes result from involvement of the main motor pathways (pyramidal tracts) of the spinal cord. Disruption of the sensory axons may produce sensory dysfunction (paresthesias, pain). Cognitive & psychosocial problems may reflect frontal or parietal lobe involvement. Involvement of the cerebellum or basal ganglia can produce ataxia (impaired coordination of movements) and tremor. Loss of control connections between the cortex and the basal ganglia may occur and cause emotional lability and euphoria. Bladder, bowel and sexual dysfunctions are common. Secondary complications: UTI, constipation, pressure ulcers, contracture deformities, dependent pedal edema, pneumonia, reactive depression & decreased bone density. Exacerbations & remissions are characteristics of MS. o Exacerbations: new symptoms appear and existing ones worsen o Remission: symptoms decrease or disappear.

Glossary

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Agnosias: loss of ability to recognize objects through a particular sensory system; may be visual, auditory or tactile.

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Akathesia: restlessness, urgent need to move around, and agitation

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Akinetic Mutism: unresponsiveness to the environment; the patient makes no movement or sound but sometimes opens the eye

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Altered level of consciousness: condition of being less responsive to & aware of environmental stimuli

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Aneurysm: a weakening or bulge in an arterial wall

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Aphasia: inability to understand language

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Apraxia: inability to performed previously learned purposeful motor acts on a voluntary basis

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Ataxia: impaired ability to coordinate movement, often seen as a staggering gait or postural imbalance

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Autonomic dysreflexia: a life threatening emergency in spinal cord injury pr that causes a hypertensive emergency; also called autonomic hyperreflexia

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Autoregulation: ability of cerebral blood vessels to dilate or constrict to maintain stable cerebral blood flow despite changes in systemic arterial BP

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Autonomic nervous system: division of nervous system that regulates the involuntary body functions.

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Axon: portion of neuron that conducts impulses away from the cell body.

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Babiski reflex (sign): a reflex action of the toes; indicative of abnormalities in the motor control pathways leading form the cerebral cortex.

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Bradykinesia: very slow voluntary movements and speech

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Brain injury: an injury to the skull or brain that is severe enough to interfere w/ normal functioning

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Brain injury, closed(blunt): occurs when head accelerates and then rapidly decelerates or collides w/ another object and the brain tissue damage, but there is no opening through the skull and dura

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Brain injury, open: occurs when an object penetrates the skull, enters the brain and damages the soft brain tissue in its path (penetrating injury), or when blunt trauma to the head is so severe that it opens the scalp, skull, and dura to expose the brain

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Brain death: irreversible loss of all functions of the entire brain, including brain stem

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Bulbar paralysis: immobility of muscles innervated by cranial nerves w/ their cell bodies in the lower portion of the brain stem

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Chorea: rapid, jerky, involuntary, purposeless movement of the extremities or facial muscles, including facial grimace

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Clonus: abnormal movement marked by alternating contraction and relaxation of a muscle occurring in rapid succession.

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Coma: prolonged state of unconsciousness

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Concussion: a temporary loss of neurologic function w no apparent structural damage to the brain

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Contusion: bruising damage to the brain surface

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Cushing response: brains attempts to restore blood flow by increasing arterial pressure to overcome the increased intracranial pressure

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Decerebration: an abnormal body posture asso w/ a severe brain injury, characterized by extreme extension of the upper and lower extremities

express

oneself

or

to

Complete spinal cord lesion: a condition involves total loss of sensation and voluntary muscle control below the lesion

Craniectomy: a surgical procedure that involves removal of a portion of the skull

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Decortications: an abnormal posture asso w/ a severe brain injury, characterized by extreme flexion of the upper and lower extremities

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Migraine headache: a severe, unrelenting headache often accompanied by symptoms such as nausea, vomiting and visual disturbances

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Delirium: transient loss of intellectual function, usually due to systemic problems

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Dementia: a progressive organic mental disorder characterized by personality changes, confusion, disorientation, and deterioration of intellect asso w/ impaired memory and judgement

Monro-Kellie hypothesis: because of limited space in the skull, an increase in any one skull component—brain tissue, blood, or CSF—will cause a change in the volume of the others

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Neurologic bladder: bladder dysfunction that results from a disorder or dysfunction of the nervous system; may lead result in either urinary retention or bladder overactivity

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Dendrite: portion of the neuron that conducts impulses toward the cell body.

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Diplopia: double vision, or the awareness of two images of the same objectoccuring in one or both eyes

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Neurodegenerative: a dse, or condtion that leads to deterioration of normal clees or function of the nervous system

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Dsyphagia: difficulty in swallowing, causing the pt to at risk for aspiration

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Neuropathy: general term indicating a disorder of the nervous system

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Dysphonia: voice impairment or altered voice production and incoordination of muscles responsible to speech

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Papilledema: edema of the optic nerve

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Dysarthria: defects neurologic causes

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Dyskinesias: impaired voluntary movements

of

articulation

due

ability

execute

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Epidural monitor: a sensor placed between the skull & the dura to monitor intracranial pressure

Parasympathetic nervous system: division of the ANS active primarily during nonstressful conditions, controlling mostly visceral functions.

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Epilepsy: a group of syndromes characterized by paroxysmal transient disturbances of brain function

Paresthesias: a sensation numbness or tingling or a “pins” and “needles” sensation

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Penumbra region: area of flow cerebral blood flow

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Expressive aphasia: inability to express oneself due; often asso w/ damage to the left frontal lobe

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Fiberoptic monitor: a system that uses light refraction to determine intracranial pressure

Persistent vegetative state: condition in w/c the pt is wakeful but devoid of conscious content, w/out cognitive or affective mental function Photophobia: inability to tolerate light

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Flaccid: displaying lack of muscle tone, limp, floppy

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Halo-vest: a lightweight vest w/ an attached halo that stabilizes the cervical spine

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Head injury: an injury to the scalp, skull, and/or brain

Primary headache: a headache for w/c no specific organic cause can be found

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Hemianopsia: blindness of half, of the field of vision in one or both eyes

Prion: a particle smaller than a virus that is resistant to standard sterilization procedures

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Hemeplegia/hemiparesis: weakness/ paralysis of one side of the body, or part of it, due to an injury to the motor areas of the brain

Radioculopathy: dse of spinal nerve root, often resulting in pain and extreme sensitivity to touch

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Reflex: an automatic response stimuli

to

to

Paraplegia: paralysis of the lower extremities w/ dysfunction of the bowel and bladder from a lesion in the thoracic, lumbar, or sacral regions of the spinal cord

Position (postural) sense: awareness of position of parts of the body w/out looking at them, also referred to as proprioception

Receptive aphasia: inability to understand what someone else is saying; often asso w/ damage to the temporal area

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Hernation: abnormal protrusion of tissue through a defect or natural opening

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Incomplete spinal cord lesion: a condition where there is preservation of the sensory or motor fibers, or both, below the lesion

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Rigidity: increase in muscle tone at rest characterized by increased resistance to passive stretch.

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Infarction: a zone of tissue deprived of blood supply

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Intracranial pressure: pressure exerted by the vol. of the intracranial contents w/in the cranial vault

Romberg test: test for cerebellar dysfunction requiring the pt to stand w/ feet together, eyes closed and arms extended; inability to maintain the position, w/ either significant stagger or sway, is a (+) test.

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Korsakoff’s syndrome: personality disorder characterized by psychosis, disorientation, delirium, insomnia & hallucination

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Sciatica: inflammation of sciatic nerve, resulting in pain and tenderness along the nerve through the thigh and leg

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Locked-in syndrome: condition resulting from a lesion in the pons in w/c the pt lacks all distal motor activity (tetraplegia) but cognition is intact.

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Secondary headache: headache identified as a symptom of another organic disorder

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Secondary injury: an insult to the subsequent to the original traumatic event

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Seizures: paroxysmal transient disturbance of the brain resulting from a discharge of abnormal electrical activity

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Spasticity: sustained increase tension of a muscle when it is passively lengthened or stretched; hypertonicity w/ increased resistance to

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Microdialysis: procedure in w/c an intracranial catheter is inserted near an injured area of the brain to measure lactate, pyruvate, glutamate and glucose levels

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Micrographia: handwrtting

small

and

often

illegible

brain

stretch often asso w/ weakness, increased deep tendon reflexes and diminished superficial reflexes

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Spinal cord injury: an injury to the spinal cord, vertebral column, supporting soft tissue or intervertebral disk caused by trauma

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Spondylosis: ankylosis or cervical or lumbar vertebrae

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Spongiform: having the appearance or quality of a sponge

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Status epilepticus: episode in w/c the pt. experiences multiple seizure bursts w/ no recovery time between

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Sunarachnoid screw or bolt: device placed into the subarachnoid space to measure intracranial pressure

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Sympathetic Nervous System: division of the ANS w/ predominantly excitatory responses, the “fight-or-flight” system

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Tetraplegia (quadriplegia): paralysis of both arms and legs, w/ dysfunction of bowel and bladder from a lesion of the cervical segments of the spinal cord

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Tone: tension present in a muscle at rest

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Transsphenoidal: surgical approach pituitary via the sphenoid sinuses

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Ventriculostomy: a catheter placed in one lateral ventricles of the brain to measure intracranial pressure and allow for drainage of fluid

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Vertigo: an illusion of movement, usually rotation

stiffening

if

the

Transaction: severing of the spinal cord itself; transaction can be complete (all the way through the cord) or incomplete (partially through) to

the