Organization of the Nervous System CENTRAL NERVOUS SYSTEM (CNS) Brain and the Spinal Cord PERIPHERAL NERVOUS SYSTEM (PN) Spinal Nerves Cranial Nerves

PNS SENSORY or AFFERENT NS conveys impulses to the CNS from sensory receptors located in various parts of the body MOTOR or EFFERENT NS carries impulses from the CNS to effectors organs, muscles and glands which brings about a response **Somatic Nervous System allows conscious or voluntary control of the skeletal muscles **Autonomic Nervous System regulates events that are automatic or involuntary; has two parts: SYMPATHETIC AND PARASYMPATHETIC

CELL BODY the metabolic center of the neuron DENDRITES conveys incoming messages toward the cell body AXONS generates nerve impulses and typically conduct them away from the cell body

Axons outside the CNS are myelinated by Schwann Cells; the outer part of the SC is called Neurillema; the gaps or indentations in regular intervals are called Nodes of Ranvier Myelin sheaths in the CNS is formed by oligodendrocytes; it doesn t have neurillema. ***when peripheral nerve is damaged neurillema plays an important role in regeneration; largely lacking in the CNS

THE BRAIN

BRAINSTEM MEDULLA OBLONGATA regulates heart rate and blood vessel diameter, breathing, swallowing, coughing, sneezing, balance and coordination. PONS controls breathing, swallowing and balance, chewing and salivation MIDBRAIN consists of 4 colliculi; 2 superior colliculi are involve in visual reflexes turning the head towards a tap on the shoulder, a sudden loud noise, a bright flash of light

Also involved in the coordination of eye movement and in control of pupil diameter and lens shape. Scattered through the BS is the Reticular Formation involved in regulating cyclical motor functions such as respiration, walking and chewing; also aids in maintaining consciousness and in regulating the sleep-wake cycle by being a part of RAS

CEREBELLUM Means little brain Involved in balance, maintenance of muscle tone, coordination of fine motor movement For smooth and coordinated movements Alcohol inhibits the function of the cerebellum

DIENCEPHALON THALAMUS most sensory input ascends through the spinal cord and brainstem projects to the thalamus influences mood and registers and unlocalized, uncomfortable perception of pain EPITHALAMUS involved in the emotional and visceral response to odors and the pineal body the pineal body is an endocrine gland that may influence the onset of puberty.

HYPOTHALAMUS maintains homeostasis plays a central role in control of body temperature, hunger and thirst sensations such as sexual pleasure, feeling relaxed and good after a meal, rage, and fear emotional responses such a nervous sweating in response to stress and hunger

CEREBRUM FRONTAL LOBE control of voluntary motor functions, motivations, aggression, mood and olfactory (smell) reception PARIETAL LOBE principal center for the reception and conscious perception of most sensory information such as pain, touch, temperature, balance and taste. OCCIPITAL LOBE reception and perception of visual input TEMPORAL LOBE involved in olfactory and auditory sensations and plays an important role in memory; also with abstract thoughts and judgment (psychic cortex)

MENINGES

MENINGES surrounds and protects the brain and the spinal cord DURA MATER most superficial and thickest Dural venous Sinuses spaces within the dura mater folds, which collects blood from the small veins of the brain; it empties into the internal jugular vein EPIDURAL SPACE the space between the dura and the periosteom; epidural anesthesia of spinal nerves in induced by injecting anesthetics into this space

ARACHNOID MATER second meningeal layer SUBDURAL SPACE the space between the dura mater and arachnoid mater PIA MATER third meningeal layer; very tightly bound to the surface of the brain and SC SUBARACHNOID SPACE the space between the arachnoid mater and pia mater which is filled with CSF and contains blood vessel

CEREBROSPINAL FLUID (CSF) Bathes the brain and SC, providing a protective cushion Produced by the Choroid Plexuses in the ventricles of the brain

The SPINAL CORD Approximate ly 17 inches or 42 cm long Has 31 spinal nerves

SPINAL NERVES Most of the spinal nerves are grouped into plexuses, where nerves come together and then separate Only T2 through T11 do not join a plexus; instead these nerves extend around the thorax between the ribs, giving off branches to muscles and skin

Plexuses of the Spinal CordPlexusCERVICAL

Origin

Major Nerves

Muscles Skin Innervated Innervated Several neck muscles DiaphragmTwo shoulder muscles Posterior arm & forearm muscles (extensors

C1 C4Phrenic

Neck and posterior head

BRACHIAL

C5 T1

Axillary

Part of the shoulder Posterior arm, forearm and hand

Radial

Musculocutaneous

Anterior arm muscles (flexors) 2 anterior forearm muscles (flexors) Most intrinsic hand muscles Medial thigh muscles (adductors)

Radial surface of the forearm

Ulnar

Ulnar side of hand

LUMBOSACRAL

L1 S4

Obturator

Medial thigh

Femoral

Anterior thigh Anterior muscles thigh, medial (extensors) leg and foot

Ischiadic (sciatic) Tibial

Posterior thigh muscles (flexors), anterior and posterior leg muscles, most foot muscles

Posterior leg and sole of foot

Common fibular

Lateral thigh and leg, some foot muscles

Anterior leg and lateral leg and dorsal or top part of foot

CRANIAL NERVES There are 2 categories of CN functions; sensory and motor The motor functions of the CN are subdivided into somatic motor and parasympathetic Somatic motor CN innervate skeletal muscles in the head and neck Parasympathetic CN innervate glands, smooth muscles and cardiac muscles.

The 12 CRANIAL NERVESNUMBER NAME GENERAL FUNCTION SPECIFIC FUNCTION

I II III

OLFACTORY

S S M,P

Smell VisionMotor to 4 of 6 eye extrinsic muscles and upper eyelid; parasympatheti c constrict pupils; thickens lens

OPTICOCULOMOTOR

IV

TROCHLEAR

M

Motor to 1 extrinsic eye muscle; follow moving objects Sensory to face and teeth; motor to muscles of mastication (chewing) Motor to 1 extrinsic eye muscles; lateral movement of the eyes

V

TRIGEMINAL

S,M

VI

ABDUCENS

M

VII

FACIAL

S,M,P

sensory: taste, motor to muscles of facial expressions; parasympathetic to salivary and tear glands

VIII

VESTIBULO COCHLEAR (ACOUSTIC) GLOSSOPHARYNGEAL

S

Hearing and balanceSensory: taste and touch to back of tongue; motor to pharyngeal muscles; PS to salivary glands

IX

S,M,P

X

VAGUS

S,M,P

Sensory to pharynx, larynx and viscera; motor to palate, pharynx and larynx; PS to viscera of thorax and abdomen

XI

ACCESSORY

M

Motor to 2 neck and upper back muscles Motor to tongue muscles

XII

HYPOGLOSSAL

M

CN I II

DYSFUNCTION Decreased sense of smell Decreased visual acuity and visual fields

INTERVENTIONS Is often accompanied by impaired taste and weight loss Frequent reorientation to environment. Position objects around client in deference to visual impairment Intermittent eye patching Lubricate eyes to protect against corneal abrasions Caution in shaving and mouth care. Choose easy to chew foods with high caloric content. Protect corneas from abrasion by using lubricant Oral hygiene. Account for decreased food intake. Cosmetic approach to hiding facial weakness. SAFETY! Move slowly to prevent nausea and emesis. Assist ambulation Maintain airway. Prevent aspiration. Swallow therapy Mobility aids. Physical therapy Maintain airway. Prevent aspiration. Swallow therapy

III Double vision (diplopia) IV,VI V Decreased facial sensation Inability to chew Decreased corneal reflexes Facial weakness and decreased taste(ant. tongue) Hearing loss, imbalance, vertigo, tinnitus Dysarthria, Dysphagia, cardiac and respiratory instability Inability to turn shoulders or turn head from side to side Dysarthria, dysphagia

VII VIII IX X XI XII

The AUTONOMIC NERVOUS SYSTEM SYMPATHETIC DIVISION prepare a person for physical activity by increasing the heart rate and blood pressure, by dilating the air passages and stimulating perspiration; also releases glucose from the liver for energy; also referred to as: the Fight or Flight response PARASYMPATHETIC DIVISION stimulates vegetative activities such as digestion, defecation and urination; and slow heart rate and respiration; pupil constriction and thickening of the lens

Actions of the Autonomic Nervous SystemEFFECTOR ORGAN Eye : pupil Heart AUTONOMIC DIVISION ACTION

sympathetic dilation of the pupil parasympathetic constriction of the pupil sympathetic dilation of coronary arteries, increased HR, increased force of contraction parasympathetic slows, heart rate, reduces contraction and conduction, constricts coronary arteries sympathetic dilation parasympathetic constriction and mucous secretion sympathetic inhibition of peristalsis and secretion parasympathetic peristalsis and secretion sympathetic relaxed; sphincter closed parasympathetic contracted; sphincter open

Bronchi Stomach and Intestines Bladder

BASIC CONCEPTS IN NORMAL NEUROLOGIC FUNCTION Oxygen supply: requires 20% of O2 in the body Glucose supply: requires 65 to 70% of glucose in the body Blood supply: the brain requires 1/3 of the cardiac output Acid-base balance: acidosis: causes cerebral vasodilation; CNS depressant; coma alkalosis: causes cerebral vasoconstriction; CNS stimulant; seizures CSF volume: Normovolume- 100-150 ml pressure:75 180 mmH2O or 0-15 mmHg glucose: 50 80 mg/dL protein: 20 50 mg/dL

Neurologic Assessment Mental Status:*orientation to three spheres: people, time

and place *memory:immediate recall: ask the client to repeat your question recent memory: ask the client about events that occurred few minutes or few hours remote memory: ask the client about events in the remote past, or historical events that can be answered by the general population

LEVEL OF CONSCIOUSNESS The most sensitive indicator of neurologic status changes LEVEL I conscious, coherent, cognitive (3 C s) LEVEL II confused, drowsy, lethargic, obtunded, somnolent LEVEL III stuporous; responds only to noxious, strong or intense stimuli (sternal pressure, trapezius pinch, pressure at the base of the nail or supraorbital area; very strong light or very loud sound) LEVEL IV - COMA

COMA LIGHT COMA response is only by grimace or withdrawing limb from pain; primitive and disorganized response to painful stimuli DEEP COMA absence of response to even the most painful stimuli

DEFINITION:technique of objectifying a clients level ofresponses;clients best response in each area is given a numerical value,and the three values is totaled for a score ranging from 3 - 15.

EYE OPENING ABILITY:Spontaneous--------------------------------------------------------(4) To voice / speech ( on request )------------------------------(3) To pain-----------------------------------------------------------------(2) None--------------------------------------------------------------------(1)

BEST MOTOR RESPONSE,UPPER LIMB:Obeys commands------------------------------------------------(6) Localizes to pain--------------------------------------------------(5) Flexor withdrawal(decorticate posturing) ---------------(4) Abnormal flexion(decerebrate posturing) ---------------(3) Extension -------------------------------------------- --------------(2) Flaccid ---------------------------------------------------------------(1)

BEST VERBAL RESPONSE:Oriented -----------------------------------------------------------(5) Confused conversation --------------------------------------(4) Inappropriate words ------------------------------------------ (3) Incomprehensible sounds ---------------------------------- (2) None ---------------------------------------------------------------- (1)

A score of 15 indicates client is awake and oriented. A score of 7 to 4 is considered coma. The lowest score is 3,client is considered in deep coma.

SENSORY FUNCTION The sensory perception is located in the parietal lobe. This enables us to perceive pressure, temperature, texture and pain The ability to perceive sensory stimuli is stereognosis The inability to perceive sensory stimuli is agnosia

MOTOR FUNCTION MOTOR CENTER (frontal lobe) is responsible for voluntary, purposeful, coordinated movements. Apraxia is inability to perform the fine motor activities. Agraphia is inability to write Cerebellum is responsible for equilibrium, sense of posture and direction. ROMBERG test is done to assess of equilibrium. The client stands with both feet together and eyes closed. Ataxia is uncoordinated movement, characterized by widebased stance and swaying manner of walking. Extrapyramidal system. It maintains balance, posture and regulates locomotion

Muscle power. Weakness (paresis), paralysis (plegia) Muscle tone. Flaccidity (hypotonicity); rigidity (hypertonicity) Muscle volume. Atrophy is loss of muscle volume; hypertrophy is increased muscle volume Movement: bradykinesia is slow muscle movement; akinesia is absence of muscle movement Coordination: assessed by FTNT

REFLEX TESTING The center for reflex act is the spinal cord The cerebral cortex determines the motor response

Types of Reflexes Superficial Reflexes *pupillary reflex - direct light is applied to the eyes; this results to pupil constriction - accommodation reflex results to constriction of pupils when gaze is shifted from a distant object to a near object - pupillary reflex are represented by PERRLA (pupils equal, round, reactive to light, accommodation)

*Corneal Reflex is elicited by touching the cornea with a wispof cotton, as the client looks towards opposite direction; blinking of the eyes occurs *Abdominal reflex results to contraction of the side of the abdomen stroked with a blunt object *Cremasteric reflex is elicited by downward stroking of the inner thigh of males; elevation of the scrotum on the same side occurs; done to unconscious pts *Anal reflex results to contraction of the anus when it is stroked with a blunt object; done to unconscious pts *Babinski reflex is elicited by stroking the sole of the foot from heel upward; plantar flexion ( - Babinski ) is the normal response Interpretation of Superficial Reflexes 0 absent + - slightly present + - normally active

DEEP TENDON REFLEX (DTR) - ankle jerk is produced by tapping thetendon of Achilles; planter flexion of the foot occurs - knee jerk (patellar reflex) is produced by tapping the quadriceps femoris, just below the patella; results to leg extension

Reflexes to Assess Meningeal Irritation - Kernig s sign. Client is placed in supine position. Flex the knee, attempt to extend the knee. Pain is experienced - Brudzinski s sign. The client is placed in supine pos. passively flex the neck, spontaneous flexion of the hips occur. This is more accurate than Kernig s

KERNIGS SIGN Present if lower leg cannot extend due to pain and spasm when client is lying supine with one leg bent over his abdomen.

BRUDZINSKIS SIGN Present if the clients hips and knees flex when he is lying supine with his head lifted towards his chest.

Oculocephalic reflex or Doll Eye Phenomenon. Demonstrated by holding theperson s eyelids open and rotating the head from side to side. Positive or normal doll s eyes is demonstrated by conjugate movement of the eyes towards the opposite side or where the pt is looking

Oculovestibular reflex or Caloric Ice Water Test. Done by irrigating the semi-circular canalsof the ear with ice water. It causes conjugate eye movement or nystagmus. It is an accurate method of assessing brainstem function

LANGUAGE AND SPEECH BROCA S AREA in the left frontal lobe. This is the motorspeech center. This enables the person to speak and make gestures. Impairment of the BA results to expressive or motor aphasia which is the inability to speak and make gestures WERNICKE S AREA in the temporal lobes. This is the auditory speech center. This enables the person to interpret sounds or language. Impairment of the WA results to receptive auditory aphasia which is the inability to understand sounds or language Global Aphasia is inability to use and understand language. Occurs when both BA and WA are impaired. Visual speech center in the Occipital lobe. This enables the person to read and interpret symbols. Impairment of the visual speech center results to alexia or inability to read

BOWEL AND BLADDER FUNCTION The Sympathetic Nervous System (SNS) which originates from the thoracolumbar segment of the spinal cord is the inhibitory impulse. Impairment of the SNS leads to bowel and bladder retention The Parasympathetic Nervous System (PNS) which originates from the carniosacral segment of the spinal cord is the motor impulse. Impairment of the PNS leads to bowel and bladder incontinence

NEUROLOGIC

DISORDERS

INCREASED INTRACRANIAL PRESSURE A condition in which the pressure of the

CSF;

blood or brain volume within the skull exceeds theupper limits for normal pressure 75 180 mmH20 or 015 mmHg

CAUSES:Space Occupying lesions (tumor, abscess, edema) Blood supply: thrombosis, embolism, aneurysm, A-V malformation CSF. Obstruction to the flow caused by brain tumor, overproduction of CSF due to tumor in the choroid plexus

SymptomsInfants: bulging fontanel, high pitch cry poor feeding, separated sutures Older children and adults: projectile vomiting, headache changes in behavior, seizures progressive decreased LOC, may become comatosed ipsilateral pupillary dilatation contralateral hemiparesis widening pulse pressure Note: Slow increases are tolerated fairly well in young children before they become symptomatic. Adults tolerate increased ICP poorly

General Assessment Restlessness. Initial sign of increased ICP Headache, nausea and vomiting, diplopia *headache is due to traction on painsensitive brain structures and on cranial nerves *vomiting results from pressure at the medulla oblongata; may be projectile *diplopia results from pressure at the CN VI (abducens) which controls the lateral movement of the eyes. It is the longest so it is vulnerable to compression

Decreased level of consciousness due to affectations of ascending reticular activating system (ARAS) Vital signs changes that results from cerebral hypoxia - systole is elevated due to increased force of cardiac contractibility -diastole remains normal or decreased due to longer time required for the heart to relax - widening of pulse pressure; more then 40 mmHg - pulse rate is slow -respiratory rate is slow due to the involvement of the medulla oblongata and pons -body temperature may be elevated or subnormal. This is due to involvement of the hypothalamus

Pupillary changes. -anisucuria is due to CN III compression. There is ipsilateral dilatation -pinpoint pupils indicate pons involvement -fixed, dilated pupils indicate uncal herniation. This causes compression of the brainstem that results to respiratory arrest Papilledema results from the compression of the optic nerve. Also known as choked disk Lateralizing sign. This is contralateral loss of motor function due to decussation of motor fibers at the level of medulla oblongata. Right brain affectations leads to left hemiplegia and vice versa

MANAGEMENTmaintain patent airway maintain fluid balance (1200-1500ml/day) LOFI position HOB elevated, 30-40 degrees prevent further increase in ICP; avoid NV, sneezing and coughing, Valsalva maneuver, over suctioning, restraints, rectal examination, enema and bending and stooping control HPN

Pharmacotherapy Hyperosmotic agents (Mannitol [Osmitrol])- to reduce cerebral edema by inducing diuresis Diuretics (furosemide[Lasix]) Corticosteroids (dexamethasone[Decadron]) antiinflammatory effect; the only corticosteroid that can pass though the blood-brain barrier Anticonvulsants Diazepam (Valium) Phenytoin (Dilantin) *administer pc *flush with 10cc PNSS after IV push to avoid crystallization SE: gum hyperplasia, sedation, hirsutism, ataxia, nystagmus, GI upset, aplastic anemia, reddish urine

Phenobarbital (Na Luminal) SE: sedation in adults, paradoxical active reaction in children, habituation Tegretol (Carbamazepine) SE: rash, ataxia, drowsiness Analgesics (small doses of codeine, stronger opiates and sedatives are C/I ) because they may cause respiratory depression and acidosis

HYDROCEPHALUSA disorder associated with excessive fluid in the brain- putting pressure on the brain forcing it against the skull and destroying the tissues. Etiology: Congenital hydrocephalus usually results from a defect, usually associated with spina bifida Acquired Hydrocephalus usually results from a space-occupying lesion, hemorrhage, intracranial infection, or a dormant developmental defect

Types of Hydrocephalus COMMUNICATING. It results from impaired absorption of CSF in the arachnoid space NONCOMMUNICATING. There is obstruction to the flow of CSF through the ventricular system.

EARLY SYMPTOMS INFANTS- enlargement of the head (increased head circumference) - bulging fontanelles, with or without enlargement of the head size, non-pulsatile - dilated scalp vein, Macewen s sign (cracked pot sound) - sutures separated, frontal bossing, setting sun sign - Irritability,

LATE SYMPTOMS- decreased mental function - delayed development - slow or restricted movement,abnormal infantile reflexes - difficulty feeding - lethargy, excessive sleepiness - urinary incontinence - brief, shrill, high-pitched cry - slow growth (child 0-5 years)

IN OLDER INFANTS AND CHILDREN- headache

- vomiting - vision changes ( sunset eyes) - crossed eyed - uncontrolled eye movements - loss of coordination - poor gait(walking pattern) - confusion or psychosis

treatment Treatment is surgical by direct removal of the obstruction and insertion of shunts to provide primary drainage of the CSF to an extracranial compartment, usually the peritoneum (ventriculoperitoneal shunt) - the major complications of shunts are infection and malfunction - other complications include subdural hematoma caused by a too rapid reduction of CSF, peritonitis, abdominal abscess, perforation of organs, fistulas, hernias and ileus - VP shunts may be used in children older than 5 years - other shunting sites include the facial vein and the subarachnoid and subgaleal spaces.

A third ventriculostomy is a non shunting procedure used to treat children with noncommunicating hydrocephalus External ventricular drainage is used in cases of persistent CSF infection Ventricular bypass may be used in older children with noncommunicating hydrocephalus caused by aqueduct stenosis or posterior fossa mass such as medulla blastoma

SEIZUREdisordersEpisodes of abnormal motor, sensory or autonomic due to abnormal electrical discharge from brain cells.

Epilepsy- chronic recurrent seizures. may be caused by infantile fever, head injury, hypertension, CNS infection, brain tumor or metastasis, drug withdrawal, stroke

TYPES OF SEIZURES Generalized Seizures major motor seizure (grand mal)

AURA(flashing lights, smells, spots before the eyes, dizziness)

shout or cry

fallTONIC-CLONIC PHASETonic phase is char by contractions Clonic phase is char by jerking movts Accompanied by dyspnea, drooling of saliva, urinary incontinence

POST-ICTAL PHASEcessation of tonic-clonic movts Char by exhaustion, headache, drowsiness, deep sleep 1-2 HRS, disorientation

Absence Seizure (Petit mal) - sudden onset (not preceded by aura), little or no tonic-clonic movt, with twitching or rolling of eyes, blank facial expression, lipsmacking; lasts a few seconds (10-20) - Febrile Seizures - common under 5yrs. of age; seizure occurs only when fever is rising; EEG is normal 2 weeks after a seizure

PARTIAL SEIZURES Psychomotor Seizure - may follow trauma, hypoxia, drug use; purposeful but inappropriate repetitive motor acts; has a psychiatric component - aura is present - char by ongoing physical activity during the time of loss of consciousness - manifested by confusion, amnesia, need for sleep Simple Partial Seizure - seizure confined to one hemisphere of the brain. no LOC; maybe motor, sensory, or autonomic symptoms Complex Partial Seizure - begins in focal area but spreads to both hemispheres; impairs consciousness; maybe preceded by an aura

Jacksonian Seizure- twitching begins at distal end of extremity, eventually involving entire extremity and possibly entire side of the body; no LOC; not commonly seen in children

Status Epilepticus- usually refers to grand mal seizures; prolonged ( repeated seizures without regaining consciousness) and unresponsive to treatment; can result in hypoxia and possible cardiac arrest

MANAGEMENTDuring seizure activity protect from injury: prevent falls, support head, decrease external stimuli, do not restrain, do not use tongue blades(may add stimuli), loosen clothing keep airway open: side lying position, suction excess mucous observe and record seizure - note any preictal aura: fear, anxiety, hallucinations, dj vu symptoms - note nature of the ictal phase: symmetry of movement, response to stimuli, LOC, respiratory pattern - note postictal response: amount of time it takes to orient to time and place; sleepiness Provide client teaching and discharge polanning need to drug therapy wear a Medic-Alert identification bracelet or carry ID availability of support groups and community agencies

Drug therapy (Anticonvulsants) Phenytoin (Dilantin)- most commonly used can only be administered with in normal saline and levels are monitored to titrate dosage; therapeutic level is 10-20 mg/dl; side effects include gum hyperplasia, hirsutism, ataxia, gastric distress, nystagmus, anemia, sedation Phenobarbital a barbiturate and its main side effects are on the CNS Tegretol (Carbamazepine) is used when seizure have not responded to other anticonvulsants Surgery to remove the tumor, hematoma or epileptic focus

HEADACHES MIGRAINE HEADACHES *strongly hereditary *more common in women *tend to occur with stress or life crisis *last for hours to days *one side of the head is more affected than the other *caused by dilatation on blood vessels in the brain

Aura of acute attack includes: - visual field defects, confusion, paresthesia, paralysis in extreme cases Associated symptoms: - NV, chills, fatigue, irritability, sweating, edema Treatment: - Ergotamine tartrate, propanolol, NSAIDs, relaxation techniques Avoid: - chocolate, nuts, onions, food seasonings

CLUSTER HEADACHES More common in older men Precipitated by alcohol or nitrate Episode clustered together in quick succession for few days or weeks with remission that lasts for months Intense, throbbing, deep, often unilateral pain begin in the infraorbital region and spread to head and neck Symptoms: -flushing, tearing of eyes, nasal stuffiness, sweating, swelling of the temporal vessels Treatment: - Narcotic analgesic IM during acute phase

TENSION HEADACHE Muscle contraction; related to tension Episodic, vary with stress Usually bilateral, involves neck and shoulders Symptoms: - sustained contraction of head and neck muscles Treatment: - narcotic analgesics (acetaminophen, propoxyphene, phenacetin (ASA)) - relaxation techniques - amitriptyline (Elavil)

CEREBROVASCULAR ACCIDENT (CVA) loss of brain functions caused by a loss of blood

circulation to areas of the brain. The specific neurologic deficits may vary depending on the location, extent of the damage, and cause of the disorder.

Disruption of the Blood Supply to the Brain Neurologic DeficitMiddle Cerebral Artery (MCA) is most commonly affected The second most frequently affected is the internal carotid artery

CAUSES THROMBOSIS The most frequent cause of CVA The most common cause of thrombosis is atherosclerosis usually affecting elderly persons Tends to occur during sleep or soon after arising Char by gradual deterioration of pts condition May occur among pts with DM or HPN EMBOLISM- the 2nd most common cause of CVA - most common affecting younger people - most frequently caused by rheumatic heart dse and myocardial infarction -symptoms occur at anytime and progress rapidly

HEMORRHAGE - may be due to HPN, subarachnoid hemorrhage, rupture of aneurysm, AV malformation, hypocoagulation TRANSIENT ISCHEMIC ATTACKS (TIA) - refers to transient cerebral ischemia with temporary episodes of neurologic status - manifestations include contralateral weakness of the lower portion of the face, fingers, hands and legs, transient dysphagia, sensory impairment - stroke in evolution refers to development of a neurologic deficit over several hours to days - completed stroke refers to a permanent neurologic deficit

SIGNS AND SYMPTOMS decreased LOC, cognitive changes increased ICP weakness or paralysis of any body area speech deficits ( dysphonia, dysarthria, aphasia) urinary/ bowel incontinence dysphagia, chewing personality changes homonymous hemianopsia

Medications Anticoagulants, Thrombolytics Anti-platelet agents; Aspirin Analgesics Antihypertensives

Surgery Carotid endarterectomy

MANAGEMENT OF CARE Maintaining peak physical health Structuring the environment Promoting socialization Promoting independent functioning Preserving the family unit

ONCOLOGIC DISORDERS OF THE BRAIN A brain tumor is a localized intracranial lesion that occupies space within the skull. A tumor usually grows as a spherical mass, but it can grow diffusely and infiltrate tissues May result to: - incrased ICP and cerebral edema - seizure activity and focal neurologic signs - hydrocephalus - altered pituitary functions

Types of Tumors GLIOMAS intracerebral brain neoplasm MENINGIOMAS benign encapsulated tumors or arachnoid cells on the meninges ACOUSTIC NEUROMAS tumor in the 8th cranial nerve (hearing and balance) PITUITARY ADENOMAS causes hormonal changes; hypo or hyperfunction of the PG ANGIOMAS composed of abnormal blood vessels; pts are at risk for hemorrhagic stroke.

assessment Frontal Lobe personality disturbance, inappropriate affect, indifference of body functions Precentral Gyrus Jacksonian seizures Occipital Lobe visual disturbances preceding convulsion Temporal Lobe olfactory, visual or gustatory hallucinations Parietal Lobe inability to replicate pictures, loss of right-left discrimination

PHARMACOLOGIC THERAPY Corticosteroids (dexamethasone) for relieving headache and altered LOC by rdeucing inflammation anf edema around tumors Osmotic diuretics (mannitol) to decrease ICP through diuresis Small doses of morphine are given in regular intervals through catheters as near as possible to the spinal segment where the pain is projected.

Collaborative Management Care of the client with increased ICP Surgery: - supratentorial craniotomy - semi-Fowler s post op - infratentorial craniotomy - flat position, turn to side, avoid supine position for the 1st 48 hours. avoid neck flexion

CRANIOCEREBRAL TRAUMA (head injury) Involves injury to the scalp, skull, and/or brain Common causes of head injury are traffic accidents, home and occupational accidents, falls, and assaults. Bicycle accidents are also a common cause of head injury-related death and disability, especially among children

Types of Head InjuryHead injuries include both injuries to the brain and those to other parts of the head, such as the scalp and skull . Head injuries may be closed or open. A closed (nonmissile) head injury is one in which the skull is not broken. A penetrating head injury occurs when an object pierces the skull and breaches the dura mater. Brain injuries may be diffuse, occurring over a wide area, or focal, located in a small, specific area. A head injury may cause a skull fracture, which may or may not be associated with injury to the brain. Some patients may have linear or depressed skull fractures..

If intracranial hemorrhage occurs, a hematoma within the skull can put pressure on the brain. Types of intracranial hemorrage include subdural, subarachnoid, extradural, and intraparenchymal hematoma. Craniotomy surgeries are used in these cases to lessen the pressure by draining off blood. Brain injury can be at the site of impact, but can also be at the opposite side of the skull due to a contrecoup effect (the impact to the head can cause the brain to move within the skull, causing the brain to impact the interior of the skull opposite the head-impact). If the impact causes the head to move, the injury may be worsened, because the brain may ricochet inside the skull causing additional impacts, or the brain may stay relatively still (due to inertia) but be hit by the moving skull (both are contrecoup injuries).

TYPES OF BRAIN INJURY Concussion A temporary loss of function due to trauma. Mild concussions are not associated with any sequelae. However, a slightly greater injury can be associated with both anterograde and retrograde amnesia (inability to remember events before or after the injury). The amount of time that the amnesia is present correlates with the severity of the injury. Cerebral concussionIs the most common head injury seen in children.

Epidural Hematoma Epidural hematoma (EDH) is a rapidly accumulating hematoma between the dura mater and the cranium. These patients have a history of head trauma with loss of consciousness, then a lucid period, followed by loss of consciousness. Clinical onset occurs over minutes to hours. Many of these injuries are associated with lacerations of the middle meningeal artery. Although death is a potential complication, the prognosis is good when this injury is recognized and treated.

Subdural HematomaSubdural hematoma occurs when there is tearing of the bridging vein between the cerebral cortex and a draining venous sinus. At times they may be caused by arterial lacerations on the brain surface. Patients may have a history of loss of consciousness but they recover and do not relapse. Clinical onset occurs over hours. A crescent shaped hemorrhage compressing the brain will be noted on CT of the head. Surgical evacuation is the treatment. Complications include uncal herniation, focal neurologic deficits, and death. The prognosis is guarded.

Cerebral ContusionCerebral contusion is bruising of the brain tissue. The majority of contusions occur in the frontal and temporal lobes. Complications may include cerebral edema and transtentorial herniation. The goal of treatment should be to treat the increased intracranial pressure. The prognosis is guarded.

Diffuse Axonal InjuryIt usually occurs as the result of an acceleration or deceleration motion, not necessarily an impact. Axons are stretched and damaged when parts of the brain of differing density slide over one another. Prognoses vary widely depending on the extent of damage.

assessment Signs and symptoms of increased ICP CSF leakage from ears and nose Battle s sign (hematoma at the mastoid process) in basilar head trauma

MANAGEMENT maintain patent airway and adequate ventilation observe for CSF leakage - (+) Testape or Dextostix test for glucose bloody spot encircled by watery, pale ring - never clean the ears or nose, suction nose unless ordered by doctor if CSF leak is present - never blow nose; HOB elevated 30 degrees as ordered - place cotton ball in the ear to absorb otorrhea, replace frequently - gently place sterile gauze pad at the bottom of the nose for rhinorrhea - observe signs of meningitis and give antibiotics as ordered prepare client for surgery as indicated - depressed skull fracture: removal or elevation of splintered bone; debridement and cleansing of area; repair of dural tear if present; cranioplasty ( if necessary for large cranial defect) - epidural, subdural hematoma: evacuation of hematoma

Craniotomy- surgical opening of skull, used to remove atumor, evacuate blood clot, control hemorrhage, relieve increased ICP Craniectomy- excision of a portion of the skull; sometimes used for decompression Cranioplasty- repair of a cranial defect with a metal or plastic plate

INTRACRANIAL SURGERY

Pre-op Care Provide emotional support, explain that the clients head will be shaved, a head is bandaged post-op, possible temporary swelling and discoloration around the eye of the affected side, possible headache Shampoo and check for infection. Shave hair. Insert Foley catheter as ordered Evaluate and record baseline vital signs and neuro checks

Post-op Care - maintain patent airway and adequate ventilationa. Supratentorial incision- HOB elevated 15-45 degrees; position on back (if intubated or unconscious) or on unaffected side; turn q2hrs to facilitate breathing and venous return b. Infratentorial incision- HOB flat or elevated 20-30 degrees; do not flex head on chest; turn to sides q2hrs using a turning sheet; check for signs of respiratory depression c. Instruct conscious client to breathe deeply but not to cough; avoid vigorous suctioning

- monitor fluid and electrolyte status- accurate I & O; restrict fluids 1500ml/day to decrease cerebral edema - infratentorial- maybe NPO for 24hrs due to possible impaired swallowing or gag reflexes

- assess dressings frequently and report any abnormalities - administer corticosteroids, anti-convulsants, stool softeners as ordered - apply ice to swollen eyelids; lubricate lids and areas around eyes withpetrolatum jelly

SPINAL CORD INJURIESSCI occurs from trauma to the spinal cord or from compression of the spinal cord due to injury to sporting structures Leading causes are MVA, acts of violence, sporting accidents

Types of SCI Complete. No impulses is carried below the level of injury; there is complete disruption of SC functions. Incomplete. Some of the spinal cord tracts are affected while others are able to carry impulses normally

SIGNS AND SYMPTOMSSPINAL SHOCK: cessation of motor, sensory, autonomic andreflex impulses and AREFLEXIA (absence of reflexes) below the level of injury. TETRAPLEGIA/QUADRIPLEGIA: (C1-C8) injury, paralysis of all four extremities; lesions above C6- causes respi. paralysis PARAPLEGIA: (T1-L4) injury, paralysis of the lower half of the body involving both legs from loss of sympathetic control of vital functions from the brain. Clients develop orthostatic hypotension, bradycardia, decreased cardiac output, loss of ability to sweat below level of injury, subnormal temperature

NEUROGENIC SHOCK: hypotensive situation resulting

Cervical SCI - above C4 fatal - tetraplegia - respiratory muscle paralysis - bowel/bladder retention Thoracic SCI - paraplegia - poor control of upper trunk - bowel/ bladder retention Lumbar SCI - paraplegia (flaccid) - bowel/bladder retention Sacral SCI - above S2/ with erection, no ejaculation - S2 S4/ no erection, no ejaculation - paraplegia - bowel/ bladder incontinence

NURSING MANAGEMENT ACUTE CARE Asses ABC; suction, tracheostomy set; jaw thrust maneuver

immobilizecervical collar, spinal boardtraction may be used to maintain alignment of the spinal column crevical thongs and halo vests are used to apply traction and immobilize the cervical spine body casts, jackets and braces are used to immobilize thoracic and lumbar fractures Prevent pneumonia and atelectasis; turn q2hrs; cough & DBE q1hr; incentive spirometry q2hrs Maintain fluid and electrolyte balance and nutrition NGT maybe inserted until bowel sounds return; IV therapy-avoid overhydration (cord edema); check bowel sounds before feeding (paralytic ileus); progress slowly from clear liquid to regular diet

prevent complications of immobility footboard/high topped sneakers to prevent footdrop; splint for quadriplegic clients to prevent wrist drop

maintain urinary elimination catheterization; increase fluids to 3000ml/day; acid ash foods maintain bowel elimination stool softeners, suppositories to prevent fecal impaction

CHRONIC CARE neurogenic bladderintermittent catheterization q4hrs & gradually progress to q6hrs; regulate fluids to 18002000ml/day a. reflex/ upper motor neuron bladder- unable to store urine very long and empties involuntarily. bladder taps stimulating trigger points to cause reflex emptying b. nonreflexive/lower motor neuron bladder- urine retention with overflow

Spasciticystretching exercises, warm tub baths, whirlpool; antispasmodics:baclofen(Lioresal), dantrolene(Dantrium), diazepam(Valium) AUTONOMIC DYSREFLEXIA- s/s: severe headache, HPN, bradycardia, sweating, goosebumps, nasal congestion, blurred vision, seizures - reflex response to stimulation of CNS; occurs above T6- stimulus: overdidtended bladder or bowel, chilling, decubitus ulcer * raise to sitting position to decrease BP * check and remove source of stimulus (catheterize, digitally remove impacted feces, reposition client) * antihypertensives- hydralazine HCL(Apresoline)

PHARMACOLOGIC MGT* Steroid therapy with Dexamethasone to prevent and reduce SC edema * Methylprednisolone sodium succinate to decrease and prevent edema and improve blood flow * Mannitol, an osmotic diuretic * Antihypertensives- hydralazineHCL (Apresoline) for autonomic dysreflexia

WHIPLASH INJURY Damage to the ligaments, vertebrae, spinal cord or nerve roots in the neck region Caused by violent hyperextension and flexion of the neck Usually results from automobile accidents There is damage to the muscles, disks, ligaments and nervous tissues of the cervical spine

assessment Pallor Weakness Gait disturbance Dizziness Nausea and vomiting Occipital headache Nuchal rigidity

Collaborative Management Bed rest Analgesics Hot packs to the neck Cervical collar

Neural Tube Defects NTD are a group of related defects of the CNS involving the cranium or spinal cord that vary from mild to severe ETIOLOGY 50% of NTD are related to nutritional deficiency, particularly folic acid deficiency The remaining cases are multifactorial

Pathophysiology: During the 3rd to 4th wk of gestation, the neural plate closes to form the neural tube that eventually forms the spinal cord and the brain. The vertebral column develop along the spinal cord Neural tube defects result from malformations of the neural tube during the embryonic development

Types of NTD ANENCEPHALY. A severe defect involving absence of the entire brain or cerebral hemispheres; the brain stem and cerebellum may be present. Total anencephaly is incompatible with life; many anencephalics are aborted or stillborn; living neonates usually survive only a few hours ENCEPHALOCELE. It occurs when the meningeal and cerebral tissue protrudes though a defect in the skull, with the occiput being the most common site. When possible, the brain is put back into the skull SPINA BIFIDA. A defective closure of the vertebral column and is th most common defect of the CNS. Spina bifida may occurs anywhere but usually occurs in the lumbosacral area. The 3 types of SB are spina bifida occulta, meningocele, and myelomeningocele.

SPINA BIFIDAA birth defect where the backbone and spinal canal do not close before birth, which allows the spinal cord and the covering membranes to protrude out of the child's back.

Causes: genetic, viral, radiation, intrauterine folic aciddeficiency

Types* spina bifida occulta * spina bifida cystica - meningocele - meningomyelocele/ myelomeningocele (75% of cases)

SPINA BIFIDA OCCULTA. Usually doesnot affect the spinal cord. External signs include dimpling of the skin, nevi, or hair tufts over a dermal sinus. This type of defect may go undetected, and most children display no neurologic signs. If they do occur, there usually is motor or sensory deficit of the lower extremities and involvement of the urinary and bladder sphincter. MENINGOCELE. It is char by a sac, which contains meninges and cerebrospinal fluid (CSF), protruding outside the vertebrae. The spinal cord is not involved, so there is usually little to no neurologic involvement MYELOMENINGOCELE. Is similar to meningocele, but the spinal cord and accompanying nerve roots are involved. It is the most common type of spina bifida. Myelomeningocele involves sensorimotor deficits, urinary and bowel problems, and possibly, hip dislocation and club foot.

Laboratory and Diagnostic Study Findings Assays of fetal amniotic fluid, ultrasonography, or maternal serum alpha-fetoprotein concentrations can help with identifying the problem prenatally Ultrasonography, computed tomography, magnetic resonance imaging, and myelography help with the evaluation of the lesion, the amount of nerve involvement, and the degree of hydrocephalus in a neonate born with myelomeningocele

MANAGEMENT prevent trauma to the sac - cover with sterile dressing soaked with normal saline - position prone or side lying - keep area free from contamination by urine or feces - inspect for signs of infection provide adequate nutrition, high fiber diet provide sensory stimulation prevent complications aid the family in coping with the disorder surgery is usually done within 48 hours after birth to lower the risk of infection, swelling, and further damage.

No treatment is indicated for spina bifida occulta unless there is neurologic damage. If a sinus is present, it may need to be closed. Meningocele requires closure as soon after birth as possible. The neonate should be monitored for hydroephalus, meningitis and spinal cord dysfunction Myelomeningocele requires a multi-disciplinary approach. There is no cure. Closure is performed within 24 hours to minimize infection and prevent further damage to the spinal cord and roots; skin grafting may be necessary. Shunting is performed for hydrocephalus and an antibiotic is initiated to prevent infection. The child will need correction of musculo-skeletal deformities and management of urologic and bowel control problems.

Cerebral Palsy CP is a group of disabilities caused by injury or insult to the brain either before or during birth, or in early infancy. It is the most common permanent disability of childhood Occur during fetal development or near the time of birth, symptoms are usually evident before age 2 and in severe cases may appear as early as three months.

Etiology: Prenatal- genetic, altered neurologicdevelopment, trauma, anoxia to mother (toxemia, rubella, accidents); Perinatal- drugs,precipitate delivery, fetal distress, breech with delay; Postnatal- kernicterus, head trauma

CLASSIFICATION OF CP Spastic CP. Most common type; may involve one or both sides of the body - hypertonicity with poor control of posture, balance and uncoordinated movement - impairment of fine and gross motor skills. Active attempts at motion increases abnormal postures and leads to overflow of movement to other parts of the body Ataxic CP. Has wide-base gait, rapid repetitive movements performed poorly, and disintegration of movements of the upper extremities when the child reaches for objects

Dyskinetic/ Athetoid CP. It involves abnormal involuntary movements that disappear during sleep and increase with stress - athetosis (wormlike movements), dyskinetic movement of mouth, drooling and dysarthria - movements may become choreoid (irregular, jerky) and dystonic (disordered muscle tone), especially when stressed and during adolescent years Mixed/ Dystonic CP. Manifested by a combination of the char of spastic and athetoid CP

Additional Manifestations: Abnormal motor performance - early dominant hand preference - abnormal and asymmetrical crawl - poor sucking - feeding problems - persistent tongue thrust Alterations of muscle tone - increased or decreased rsistance to passive movements - child feels stiff when handling or dressing - difficulty in diapering or opisthotonos

Abnormal postures - scissoring legs - persistent infantile posturing Reflex abnormalities - persistent primitive reflexes such as tonic neck or hyperreflexia

MANAGEMENT Supportive (occupational and physical therapy, braces, appropriate glasses and hearing aids) Mainstreaming Cerebral palsy- support group Medications (muscle relaxants, anticonvulsants) Surgery

TAY-SACHS DISEASE an autosomal recessive disorder found predominantly in Jewish families, which results in early death. caused by a deficiency of hexosaminidase A, an enzyme that is important in the metabolism of gangliosides- these fatty acids then accumulate in the brain causing degenerative neurological deterioration onset: 3 to 6 months old Signs & Symptoms loss of motor skills increased startle reaction decreased eye contact (blindness); deafness listlessness; irritability seizures; dementia paralysis; loss of muscle strength delayed mental and social skills slow growth enzyme analysis of blood/body tissue for hexosaminidase levels eye exam reveals a cherry-red spot in the macula

REYES SYNDROMEIt is an acute multi system disorder that follows a mild viral infection Unknown cause, but can be associated with viral agents such as influenza or varicella, toxins, aspirin and other salicylates, and metabolic defects

Pathophysiology:The disorder is char by encephalopathy and fatty degeneration of the liver . Cell mitochondria are injured and become large and swollen, causing cerebral edema and fatty infiltration of the liver, kidneys and heart Hyperammonia results from a reduction in the enzyme that converts ammonia to urea.

stage I: sudden onset of persistent vomiting, fatigue, liver dysfunction stage II: behavior changes, disorientation, confusion, hyperreflexia, combativeness, hallucinations, hyperventilation stage III: coma, decorticate posturing, hyperventilation stage IV: deeper coma, decerebrate posturing, large fixed pupils, evidence of brainstem dysfunction stage V: seizures, absent deep tendon and respiratory reflexes, flaccid paralysis

Laboratory and diagnostic study findingsLiver function tests will detect elevated liver enzymes elevated serum ammonia test Coagulation Studies will show prolonged prothrombin time Liver biopsy is performed only if the diagnosis is unclear

MANAGEMENT Monitor the child for increased ICP Administer the prescribed medication: a druginduced coma may result when phenobarbital or pentobarbital with pancuronium (pavulon) is given to paralyze skeletal muscles, hypoglycemia is controlled with hypertonic glucose and saline solution; vitamin K may be given to correct normal clotting. Maintain a patent airway. The child is usually on a ventilator Control hypothermia.

OBS A general term refers to physical disorders that cause a decrease in mental function, usually not including psychiatric disorders Organic brain syndrome (OBS), also known as organic brain disease (OBD) or organic brain disorder, is an older and nearly obsolete general term from psychiatry, referring to many physical disorders that cause impaired mental function.[1] It usually does not include psychiatric disorders. Originally, the term was created to distinguish physical (termed "organic") causes of mental impairment from psychiatric (termed "functional") disorders, but this division became increasingly difficult to make as the physical correlates of mental problems become more numerous. Thus, the term (which was never welldefined) is now almost officially obsolete term in psychiatry, having been removed from DSM-IV, but still occasionally used in practice and in the literature.

Acute organic brain syndrome is (by definition) a recently appearing state of mental impairment, as a result of intoxication, drug overdose, infection, pain, and many other physical problems affecting mental status. In medical contexts, "acute" means "of recent onset". As is the case with most acute disease problems, acute organic brain syndrome is often temporary however this is not guaranteed (a recent-onset problem may continue to be chronic or long term). A more specific medical term for the acute subset of organic brain syndromes is delirium.[2]

Chronic organic brain syndrome is long-term. For example, some forms of chronic drug or alcohol dependence can cause organic brain syndrome due to their long-lasting or permanent toxic effects on brain function.[3] Other common causes of chronic organic brain syndrome sometimes listed are the various types of dementia, which result from permanent brain damage due to strokes, Alzheimer's disease, or other damaging causes which are not reversible. Though OBS is a common diagnosis in the elderly, like the various types of dementias it is related to a disease processes and is not an inevitable part of aging. In some of the older literature, there was an attempt to separate organic brain syndrome from dementia, but this was related to an older world view in which dementia was thought to a part of normal aging, and thus did not represent a special disease process. The later identification of various dementias as clear pathologies is an example of the types of pathological problems discovered to be associated with mental states, and is one of the areas which led to abandonment of all further attempts to clearly define and use OBS as a term.

Types Acute - delirium - clouding of consciousness - temporary alteration of brain functioning - reversible Chronic - dementia - senility - insidious onset - irreversible

a degenerative disorder of the brain cells (cerebral cortex) resulting to: - microscopic plaque (beta amyloid) - impaired intellectual function destruction of nerve cells which leads to a decrease and imbalance of neurotransmitters early onset (5-10% of cases) -symptoms first appear before age 60 late onset (most common) -develops in people 60 and older most common cause of dementia Incidence is equal among men and women

The neurons of the frontal and medial lobes are affected, with resultant biochemical and structural changes. The cells most affected that neurons that use acetylcholine neurotransmitter. The size of the brain and the mount of neurotransmitter also decrease

causes Unknown Autoimmune Heredity

stages Stage 1. mild memory lapses (forgetfulness) often subtle - indecisiveness, increasing self-centeredness, decreasing interest in others, environment and social activities - difficulty in learning new information, slowed reaction time - beginnings of compromised performance t home and at work

Stage 2. progressing forgetfulness, inability to remember names of family members pr close friends - tendency to lose things, confusion, fearfulness - easily induced frustration and irritability, sometimes angry outburst - repetitive storytelling, inability to remember words - inability to follow simple instructions, difficulty calculating numbers - getting lost in familiar places - pacing, wandering - changes in sleep-rest cycle (frequent activity at night) - neglect ADL, personal hygiene - losses of social behaviors - paranoia

Stage 3. inability to communicateInability to eat Incontinence (urine and feces) Inability to recognize family or friends Confinement to bed Total dependence to caregivers

Collaborative Management Protect from injury Promote activity Promote sleep Avoid agitation/ violence Avoid fatigue Avoid scolding/ embarrassing Avoid arguing/ reasoning Address by name

MedicationsAntipsychotic, sedatives, antianxiety agents and antidepressant may be used to treat behavioralsymptoms

Given to increase cognitive functions:

tacrine (Cognex) donepezil (Aricept) rivostigmine (Exxelon)

Paralysis Agitans 50-60 years Male> female progressive deterioration of the basal ganglia and the extrapyramidal area; deficiency of dopamine

pathophysiologyDestruction of the dopaminergic neuronal cells in the substantia nigra in the basal ganglia

Depletion of dopamine stores

Degeneration of the dopaminergic nigrostriatal pathway

Imbalance of excitatory (acetylcholine) and inhibiting (dopamine) neurotransmitters in the corpus striatum

Impairment of extrapyramidal tracts controlling complex body movements

tremors

rigidity

bradykinesia

Postural changes

assessment Pinrolling tremors of the fingers Resting tremors (non-intentional tremors) Rigidity with muscle weakness - bradykinesia/akinesia - cogwheel rigidity - absence of arm swing in normal rhythmic gait Masklike appearance of the face Drooling of saliva Dysphagia Shuffling, festinating gait (walking in tiptoe, staring in slow pace which keeps on increasing until the client assumes a running pace. The client is unable to stop unless obstruction is met)

Trunk bent forward Moist oily, skin Defects in judgment Fatigue Microphonia, slow monotonous voice Micrographia, small hand writing No intellectual impairment No true paralysis No loss of sensation Dx test: EEG, CT scan to rule out neurologic disorders, no definitive Dx test for PD.

COLLABORATIVE MANAGEMENT Diet. inc residue, inc calorie, soft well balanced diet Position to prevent contractures - firm bed, no pillows - prone position when lying in bed - hold hands folded at the back when walking Aspiration precaution

medications Anticholinergics to reduce tremors. Cogentin (Benztropine Mesylate) Artane (trihexyphenidyl) Akineton (biperiden) Side effects: *blurring of vision *dryness of mouth/throat *constipation *urinary retention *dysarthria *mental disturbance

Anti-Parkinsonian Agents (Dopaminergics). Improves muscle flexibility *Levodopa *Carbidopa w/ Levodopa (Sinemet).Carbidopa reduces destruction of Levodopa at the pariphery

Antiviral / Dopamine Agonists - Amantadine HCl (Symmetrel) - Bromocriptine (Parlodel) Antispasmodics. Procyclidine HCl(Kemadrin) Antihistamines. Diphenhydramine (Benadryl) to decrease tremors and anxiety

Avoid the ff drugs when on Levodopa therapy: - phenothiazines, reserpine, pyridoxine (vit. B6) which block the effect of Levodopa. - MAOI (parnate, marplan, nardil) * enhances norepinephrine activity * may cause hypertensive crisis * methyldopa potentiates the effects of Levodopa

Avoid the ff foods when on levodopa therapy: - B6 rich foods: tuna, pork, dried beans, salmon, beef liver (block the effect of levo) - tyramine rich foods (may cause hypertensive crisis: cheese, cream, yogurt, coffee, chocolate bananas, raisins, liver, sausage, soy sauce yeast, beer, red wine

SIDE EFFECTS OF LEVODOPA Nausea and vomiting Orthostatic hypotension Insomnia Agitation Mental confusion Renal damage Reddish brown urine

Huntingtons Disease It is a chronic, progressive, hereditary disease of the NS that results in progressive involuntary choreiform movements and dementia. Affects both sexes of all races at midlife It is transmitted as an autosomal dominant genetic disorder

pathophysiology It involves premature death of brain cells in the striatum of the basal ganglia, the region deep within the brain that controls movement Cells are also lost in the cortex, the region of the brain involved in thinking, memory, perception and judgment It also affects the cerebellum, the area that coordinates voluntary muscle movement

Clinical Manifestations Chorea (abnormal involuntary movements) Intellectual decline Emotional disturbance Writhing, twisting, uncontrollable movement may involve the entire body Facial movements produce tics and grimaces Speech becomes slurred, hesitant, often explosive and eventually unintelligible Chewing and swallowing are difficult Gait becomes unorganized to the point that ambulation becomes impossible Hallucinations, delusions, and paranoid thinking may precede the appearance of disjointed movements.

The Diagnosis is made based on the clinical presentation of characteristic symptoms, a positive family history, the known presence of a genetic marker and exclusion of other causes.

management No treatment halts or reverses the disease Thiothixene hydrochloride (Navane) and Haloperidol decanoate (Haldol)- block dopamine receptors, improve the chorea in many patients Several new treatments such as fetal tissue transplantation and the use of growth factor delivered to the basal ganglia region of the brain are under investigation

20-40 years Female>male Impaired nerve impulse conduction because of destruction of myelin sheath

pathophysiologyCauses: unknown, autoimmune, viral infectionMultiple foci of demyelinization in the white matter (brainstem, spinal cord, optic nerves, cerebrum) then later the gray matter

Destruction of the myelin sheath (Schwanns cells) Interruption/distortion of impulse (slowed/blocked)

Signs and Symptoms- diplopia (double vision) - scotoma (spots before the eyes) - muscle spasticity - poor coordination - speech deficits - intentional tremor - bowel/ bladder dysfunction - exacerbations and remissions - dysphagia - ataxic gait

CHARCOATS TRIAD scanning speech intention tremors nystagmus LHERMITTES SIGN. Sudden electrical shock sebsation on passive flexion of the neck

Eye patch for diplopia Diet should be well balanced and high in fiber to prevent constipation Avoid hot baths. Heat increases weakness Plasmapheresis Muscle relaxants: (Baclofen, dantrolene, diazepam) Glucocorticoids: prednisone dexamethasone corticotropin Cholinergic medications Amantadine; Antidepressant

Collaborative Management

Lou Gehrigs disease A motor neuron dse 40-70 years Male>female ;inc in middle aged men Impaired nerve impulse conduction because of degeneration of motor neurons

pathophysiologyMyelin sheath destruction

Scar tissue formation

Blocking/ distortion of Nerve Impulses

Causes: unknown viral infection

Signs and symptoms- fatigue - awkwardness of fine fingers movement - muscle weakness, progressing to atrophy and paralysis of upper and lower extremities - impaired speech; hoarseness - difficulty swallowing and breathing - jaw clonus - muscle contractions; twitching - usually fatal 2-15years after onset Brainstem, medulla oblongata involvement

Death: 5-10 year (respiratory paralysis) Diagnostic Test: EMG (no definitive test)

Collaborative Management Gastrostomy feeding Assist with ADL Prosthesis to support weakened muscles Promote effective airway Tucked chin when eating and drinking to facilitate swallowing Antibiotics( for respiratory and urinary infections)

Medication

A neuromuscular disorder that results in the failure to transmit nerve impulses at the myoneural junction 20-50 years Female>male Impaired transmission of nerve impulse to muscle cell possibly because of acetylcholine deficiency 25% with THYMOMA

causes Decreased ACETYLCHOLINE secretion by the motor end plate Increased cholinesterase at the nerve endings Autoimmune diseases

Signs and Symptoms- vision changes - profound muscle weakness or paralysis that worsens with exertion later in the day - fatigue - PTOSIS - diplopia - impaired speech - strabismus - gnarl smile (smiles slowly) - masklike facial expression - drooling - difficulty talking; dysphagia; dyspnea; frequent choking - can progress to respiratory failure(myasthenia crisis)

DIAGNOSTIC TEST TENSILON TEST. Edrophonium Chloride Test* tensilon is a short acting cholinergic is administered * increased muscle strength is observed (+Tensilon test) * it is important that the client does not know when the medication is given to obtain true results

Collaborative Management Assess swallowing/ gag reflex before feeding the pt Administer medication 20-30 mins a.c. to prevent aspiration Administer medications at precise time to prevent respiratory distress Start meal with cold beverages to improve ability to swallow Avoid exposure to infection Plasmapheresis. This involves removal of antibodies from the plasma to inhibit autoimmune response

Pharmacotherapy: cholinergics (anticholinesterase) - neostigmine (prostigmin) - pyridostigmine (mestinon) - ambenomiun (mytelase) Glucocorticoids. For anti0inflammatory effects Antacids. To prevent GI upset due to glucocorticoids

Surgery:Thymectomy. This achieves remission for 5-10 years

Drugs to be Avoided by Client with MG: Muscle relaxants Barbiturates Morphine sulfate Tranqulizers Neomycin (potentiates muscle weakness because of its effect on myoneural function)

COMPLICATIONMyasthenia Crisis- abrupt onset of severe, generalized muscle weakness with inability to swallow, speak or maintain respirations - caused by undermedication, physical or emotional stress, infection - symptoms will temporarily improve with Tensilon test

Cholinergic Crisis- same symptoms to myasthenia crisis; side effects of anticholinesterase drugs (excessive sweating and salivation, abd. cramps, diarrhea, fasciculations, N & V) - caused by overmedicaiton with the cholinergic (anticholinesterase) drugs - symptoms worsen with Tensilon test; keep atropine sulfate and emergency equipment on hand

Infectious Polyneuritis A rare dse affecting the peripheral and cranial nerves May occur at any age but is most common in people of both sexes; between the ages 30 and 50. Acute inflammation damages portions of the nerve cell, resulting in muscle weakness or paralysis; (demyelination and denervation) Usually follows a viral infection (usually respiratory or gastrointestinal) ; may be autoimmune; may follow swine flu immunization

Signs and Symptoms- Weakness begins in the feet and legs and may progress upward to the arms and cranial (head) nerves (ascending paralysis) - May progress rapidly over 24 to 72 hours - May begin in the arms and progress downward (descending paralysis) - May progress to respiratory paralysis - Numbness, decreased sensation - Tenderness or muscle (may be a cramp-like pain) - Drooling, difficulty swallowing and breathing - Urinary dysfunction

Management There is no specific management Symptomatic; supportive care of paralyzed, immobilized pts. Mechanical ventillation; Corticosteroids; Plasmapheresis

TRIGEMINAL NEURALGIA (Tic Douloureux) A neurologic disorder affecting the 5th cranial nerve Manifested by excruciating, recurrent paroxysms of sharp, stabbing pain along the trigeminal nerve Caused by vascular compression and pressure; as the brain changes w/ age, a loop of cerebral artery or vein may compress the nerve root entry point.

Occurs most often before 35 yerars of age and most common in women and in people w/ MS Paroxysms can occur with any stimulation such as washing of the face, shaving, brushing of teeth, eating and drinking; even a draft of cold air or direct pressure against the nerve trunk

Signs and Symptoms Involuntary contractions of the facial muscles. Sudden closing of the eye or twitching of the mouth (tic couloureux painful twitching)

Phramacologic therapy Antiseizure agents. Carbamazepine (Tegretol) to relieve pain. To be taken w/ meals SE: nausea, dizziness, drowsiness, aplastic anemia Gabapentin (neurontin) and baclofen (lioresal) are also used to control pain If pain is still not controlled Phenytoin (Dilatin) may be used as adjunctive therapy

Management Alcohol injection of the nerve Surgery (neurectomy); microvascular decompression Percutaneous Balloon Decompression Avoid extremes of heat and cold Protect eye if surgery is done

BELL]S PALSY Lower motor neuron lesion or inflammation of the 7th cranial nerve resulting to paralysis of the side of the face Usually self-limiting to a few weeks Theoried to be caused by vascular ischemia, viral dse (herpes simplex, herpes zoster), autoimmune dse or a combination of all the factors

manifestations Facial paralysis involving the eye (ptosis) Tearing of eye Speech and eating difficulties Painful sensations in the face Sagging of one side of mouth, drooling

management Steroids (prednisone) to reduce inflammation and edema; this reduce the vascular compression and permits restoration of blood supply to the nerve Analgesics Heat may also be applied Electrical stimulation may also be used top prevent muscle atrophy Protect involved eye Active facial exercises ( wrinkling of forehead, whistling)

LYMES DISEASE Lyme disease, or lyme borreliosis, is an emerging infectious disease caused by at least three species of bacteria belonging to the genus Borrelia. Borrelia burgdorferi sensu stricto[4] is the main cause of Lyme disease in the United States, whereas Borrelia afzelii and Borrelia garinii cause most European cases. The disease is named after the town of Lyme, Connecticut, USA, where a number of cases were identified in 1975.

Lyme disease is the most common tickborne disease in the Northern Hemisphere. Borrelia is transmitted to humans by the bite of infected ticks belonging to a few species of the genus Ixodes ("hard ticks").

SIGNS AND SYMPTOMS Early symptoms may include fever, headache, fatigue, depression, and a characteristic circular skin rash called erythema migrans. Left untreated, later symptoms may involve the joints, heart, and central nervous system. In most cases, the infection and its symptoms are eliminated by antibiotics, especially if the illness is treated early. Delayed or inadequate treatment can lead to the more serious symptoms, which can be disabling and difficult to treat. Lyme disease is a biosafety level 2 disease.

STAGES OF MANIFESTATIONSTAGE 1: Early localized infectionCommon bulls-eye rash pattern associated with Lyme disease also called erythema chronicum migrans

Stage 2: Early disseminated infection Within days to weeks after the onset of local infection, the borrelia bacteria may begin to spread through the bloodstream. Symptoms may include migrating pain in muscles, joint, and tendons, and heart palpitations and dizziness caused by changes in heartbeat. Various acute neurological problems, termed neuroborreliosis, appear in 10 15% of untreated patients. These include facial palsy, which is the loss of muscle tone on one or both sides of the face, as well as meningitis, which involves severe headaches, neck stiffness, and sensitivity to light. Radiculoneuritis causes shooting pains that may interfere with sleep as well as abnormal skin sensations. Mild encephalitis may lead to memory loss, sleep disturbances, or mood changes.

STAGE 3: Late persistent infection Deer tick life cycle After several months, untreated or inadequately treated patients may go on to develop severe and chronic symptoms that affect many parts of the body, including the brain, nerves, eyes, joints and heart. Myriad disabling symptoms can occur, including permanent paraplegia in the most extreme cases.

treatment Antibiotics are the primary treatment for Lyme disease; the most appropriate antibiotic treatment depends upon the patient and the stage of the disease.

Doxycycline (in adults), amoxicillin (in children), erythromycin (for pregnant women) and ceftriaxone, with treatment lasting 10 to 28 days. Alternative choices are cefuroxime and cefotaxime. Treatment of pregnant women is similar, but tetracycline should not be used. In later stages, the bacteria disseminate throughout the body and may cross the blood-brain barrier, making the infection more difficult to treat. Late diagnosed Lyme is treated with oral or intravenous antibiotics, frequently ceftriaxone for a minimum of four weeks. Minocycline is also indicated for neuroborreliosis for its ability to cross the blood-brain barrier.

Meningitis- inflammation of the meninges of the brain and spinal cord, caused by bacteria, viruses, or other microorganisms. Encephalitis- inflammation of the brain, caused by a virus; may occur as a sequela of measles, mumps, chickenpox. Signs and symptoms: headache, photophobia, irritability, chills, fever, vomiting possible seizures,decreasing LOC signs of meningeal irritation - nuchal rigidity: stiff neck - opisthotonos: head and heels bent backward and body arched forward - Kernigs sign - Brudzinkis sign Tests: Lumbar puncture- measurement and analysis of CSF shows increased pressure, elevated WBC and protein, decrease glucose and culture positive for specific microorganism.

CNS INFECTIONS

give large doses of antibiotics as ordered enforce respiratory isolation after initiation antibiotic therapy for some types of meningitis give nsg. care for increased ICP, seizures, and hyperthermia provide nsg. Care for delirious or unconscious client as needed bed rest; keep room quiet & dark if photophobia or headache occurs maintain fluid and electrolyte balance prevent complications of immobility monitor vital signs and neuro checks frequently teach client concerning discharge plans: - maintain a good diet high in protein, high calories, with small frequent feedings - rehabilitation program for residual deficits

MANAGEMENT