Acute Neurologic Disorders2

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Acute Neurologic Disorders

Review of the NS

Brain

I. Definition

The communication and control center of the body

Receives, processes and evaluates many kinds of input ; decides on the

response to be taken ; and then initiates the response

Responses :

o

Involuntary activity regulated by autonomic nso

Voluntary actions regulated by somatic ns

II. Protection for the Brain

Protected by :

o

Skull

o 3 membranes / meninges

o CSF Sutures :

o Immovable joints consisting of fibrous tissue

o Cranial and facial joints are connected by thiso If pressure inside the skull increases in infants before sutures

fuse or ossify , cranial bones may separate causing the head toenlarge

Foramina :

o

Cavities /Openings in skullo

Canals through which nerves and blood vessels pass

o Largest opening is the Foramen magnum , located in theoccipital bone @ the base of the skull where the spinal cord

emerges

Meninges

Consists of 3 connective tissue membranes covering the brain and

spinal cord

Invaginate @ 4 points forming a supportive partition bet portions of

brain :o Falx cerebri

- extends downward into the longitudinal fissure (deepgroove) bet the cerebral hemispheres

o Tentorium cerebelli

- separates the cerebral hemispheres from the cerebellum

Dura mater

o Outer layer

o

Tough, fibrous, double-layered membrane that separates @

specific points to form the dural sinuses w/c collect venous

blood and CSF for return to the general circulation

Subdural space

o Lying beneath the dura

o

A potential space i.e normally empty, could fill with blood

after an injury Arachnoid

o Middle layer

o Loose, web-like covering

Subarachnoid space

o Contains the CSF and cerebral arteries and veins

o Lies beneath the arachnoid

Arachnoid villio Projections of arachnoid into the dural sinuses @ several

places around brain through w/c CSF can be absorbed intothe venous blood

Pia mater

o

Inner layer

o Delicate connective tissue

o Adheres closely to all convolutions on the surface of the braino

Many small blood vessels can be found

CSF

Provides a cushion for the brain and spinal cord

Clear, almost colorless liquid

Concentrations of electrolytes, glucose and protein remain relatively

constant

Characteristics :

o

Appearance – clear and colorless

o Pressure – 9 to 14 mm Hg or 150 mm H20

o RBC - Noneo

WBC – Occasional

o Protein – 15 to 45 mg/dL

o Glucose – 45-75 mg/dLo Sodium – 140 mEq/L

o Potassium – 3 mEq/L

o

Sp. gravity – 1.007

o pH – 7.32 to 7.35

o

Volume in the system @ one time – 125 to 150 mLo Volume formed in 24 h – 500 to 800 mL

Change in the characteristic is a useful diagnostic tool

Formed constantly in the choroid plexuses in the ventricles and then

flows into the subarachnoid space where it circulates around the

brain and spinal cord and eventually passes through the arachnoid

villi , returning into the venous blood To maintain a relatively constant pressure within the skull

(intracranial pressure) , it is important for equal amt of CSF to be

produced and reabsorbed @ the same rate

Present throughout the brain except where the presence of sensory

receptors for regulation of body fluids requires normal diffusion (egosmoreceptors in hypothalamus)

Blood-brain barrier

Protective mechanism provided primarily by relatively impermeablecapillaries in the brain

Endothelial cells of the capillaries are tightly joined together rather

than possessing pores Limits the passage of potentially damaging materials into brain and

controls delicate but essential balance of electrolytes, glucose, and

proteins in brain

Poorly developed in neonates and therefore substances such as

bilirubin , Rh factor incompatibility or other toxic materials can passeasily into infant’s brain , causing damage

When fully developed , it can be a disadvantage because it does not

allow the passage of many essential drugs into brain Lipid-soluble substances including some drugs and alcohol , pass

freely into brain

Blood-CSF barrier

@ choroid plexus Control constituents of CSF

III. Functional Areas

Cerebral hemispheres Make up the largest and most obvious portions of the brain

Outer surface is covered by elevations (gyri) that are separated by

grooves (sulci)

The longitudinal fissure separates the 2 hemispheres

The surface (cortex) consists of gray matter / nerve cell bodies

White matter :

o Beneath the gray matter

o Composed of myelinated nerve fibers bundled into tracts

w/c :

- connect the hemispheres (corpus callosum)- occur as projection fibers , connecting the cortex to thespinal cord

- occur as association fibers, connecting diff gray areas inthe brain

Each hemisphere

o Divided into 4 major lobes , each of w/c has some specificfunctions

o Concerned with voluntary movements and sensory function inthe opposite (contralateral) side of the body

Upper motor neurons (UMNs)

o Cells of the motor cortex of the frontal lobe w/c initiatespecific voluntary movements

o Their axons form the corticospinal tracts in the spinal cord



o Because the crossover of most of these tracts occurs inmedulla, damage to the motor cortex in L frontal lobe

adjacent to the longutidinal fissure (on top of head) results

paralysis / paresis of muscles of the R leg

Each special sensory area of the cortex has an association area

surrounding primary cortex in w/c sensory input is recognized and

interpretedo Primary visual cortex receives stimuli from the eye

o Surrounding association cortex identifies the object seen

o

If primary cortex is damaged :

- person is blind

o

If association area is damaged :- person can see the object but cannot comprehend its

significance

Basal nuclei

o Sometimes called the basal ganglia

o

Clusters of cell bodies or gray matter

o Located deep among the tracts of the cerebral hemispheres

o Part of the extrapyramidal system (EPS) of motor control

w/c controls and coordinates skeletal muscle activity,

preventing excessive movements and initiating accessory andoften involuntary action

o

2 additional nuclei located in the midbrain : (also connected

to basal nuclei and EPS)- substantia nigra

- red nucleus

Limbic system

o

Consists of many nuclei and connecting fibers in the cerebralhemispheres that encircle the superior part of the brain

stem

o Responsible for emotional reactions or feelings and for this

purpose, it has many connections to all areas of the braino

Part of hypothalamus is involved with limbic system , it

provides link for autonomic responses such as altered BP ornausea that occur when one experiences fear, excitement,

or an unpleasant sight or odor

o Any cognitive (intellectual) decision arising from higher

cortical centers may be accompanied by an emotional aspet

mediated through limbic system

Dominant hemisphere / L hemisphere Side of the brain that controls language

2 special areas involved in language skills :

o

Broca’s area- the motor or expressive speech area- the output of words, both verbal and written is

coordinated in an app and understandable way

- located @ the base of the premotor area of the L frontal

lobe

o

Wernicke’s area

- comprehends language received , both spoken and written

- located in the posterior temporal lobe- has connecting fibers to the prefrontal, visual, and

auditory areas

Also responsible for :

o Mathematical

o Problem-solving

o

Logical reasoning

Right Hemisphere

Has greater influence on :

o Artistic abilities

o

Creativity

o Spatial relationships

o Emotional and behavioral characteristics

4 major Lobes of each hemisphere

Frontal Lobe

o Prefrontal area – intellectual function and personality

o Premotor cortex – skilled movementso

Motor cortex – voluntary movements

o Broca’s area – speech (expression)

Parietal Lobe

o Somatosensory area – sensation

Occipital Lobe

o Visual cortex - vision Temporal Lobe

o

Auditory cortex - hearing

o Olfactory cortex – smell

o

Wernicke’s area - comprehension of speech ; memory

Diencephalon

Central portion of the brain

Surrounded by the hemispheres

Contains the thalamus and hypothalamus

Thalamus

Consists of many nerve cell bodies

Serve as a sorting and relay station for incoming sensory impulses

Connecting fibers transmit impulses to the cerebral cortex and

other app areas of brain

Hypothalamus

Has a key role in maintaining homeostasis

o

Controlling autonomic NS and much of endocrine system

through hypohysis / pituitary gland

o Regulation of body temp

o

Intake of food and fluid

o Regulation of sleep cycles

Also key to the :

o

Stress responseo Emotional responses through limbic system

o Biologic behaviors (eg. sex drive [libido])

Brainstem Inferior portion of the brain

Connecting link to the spinal cord

Pons

Composed of bundles of afferent (incoming) and efferent (outgoing)

fibers

Several nuclei of cranial nerves are also located here

Medulla oblongata

Contains the :

o Vital control centers that regulate respiratory andcardiovascular function

o

Coordinating centers that govern cough reflex, swallowing andvomiting

Location of the nuclei of several cranial nerves Distinguished by 2 longitudinal ridges on the ventral surface termed

pyramids , marking the site of crossover (decussation) of the

majority of fibers of corticospinal (pyramidal) tracts w/c results in

contralateral control of muscle function

Reticular formation

Network of nuclei and neurons scattered throughout the brainstem

Has connections to many parts of the brain

RAS/ Reticular-activating system o Determines the degree of arousal or awareness of the

cerebral cortex

o

Neurons decide w/c of the incoming sensory impulses the

brain ignores and w/c it noticeso Many drugs can affect the activity of the RAS thus

increasing or decreasing input to the brain

Cerebellum

Located dorsal to the pons and medulla , below the occipital bone

Functions to coordinate movement and maintain posture and

equilibrium by continuously assessing and adjusting input from:o

Pyramidal system

o Prorioceptors in joints and muscles

o

Visual pathways and vestibular pathways from inner ear



IV. Blood Supply to the Brain

Blood is supplied to the brain by the internal carotid arteries and

vertebral arteries

Each internal carotid artery is a branch of a common carotid artery (R

or L) and includes the carotid sinus

Carotid sinus :

o Location of pressoreceptors/Baroreceptors that signal

changes in BP

o

Also of chemoreceptors that monitor variations in blood pH

and O2 levels

At the base of brain, each internal carotid artery divides into ananterior and middle cerebral artery

o Anterior cerebral artery – supplies the frontal lobeo

Middle cerebral artery – supplies the lateral part of cerebral

hemispheres ,primarily temporal and parietal lobes

Posteriorly , the vertebral arteries join to form :

o Basilar artery – supplies branches to brainstem and cerebellum

as it ascends

At the base of the brain , basilar artery divides into :

o R and L posterior cerebral arteries - supply blood to theoccipital lobe

Anastamoses bet. the major arteries at the base of brain are provided

by the :

o

Anterior communicating artery – bet. the anterior cerebral

arteries

o Posterior communicating arteries – bet. the middle cerebral

and posterior cerebral arteries Circle of Willis

o The arrangement of arteries and anastamoses

o Provides an alternative source of blood when internal carotid or

vertebral artery is obstructedo

Surrounds the pituitary gland and optic chiasm

Blood flow in cerebral arteries is relatively constant because brain

cells constantly use O2 and glucose and have little storage capacity

Autoregulation

o Mechanism by w/c increased CO2 levels or decreased pH in

blood or decreased BP in an area of brain results in immediate

local vasodilation

o The pressoreceptors and chemoreceptors protect brain from

damage r/t abnormal BP or pH levels in systemic flow Venous blood from brain collects in dural sinuses and then drains into R

and L internal jugular veins, to be returned to the heart

V. Cranial Nerves

There are 12 pairs

Originate from the brainstem Pass through the foramina in the skull to serve structures in the head

and neck The vagus nerve :

o

Serves a more extensive area

o Branching to innervate many of the viscera

May consist of :

o Motor fibers

o Sensory fibers

o

Mixed nerve (both motor and sensory)

4 cranial nerves (III, VII, IX, X) include parasympathetic fibers



Spinal Cord and Peripheral Nerves

I. Spinal cord

Protected by :

o

Bony vertebral column

o Meninges

o

CSF

Continuous with medulla oblongata Ends @ the level of first lumbar vertebra

Cauda equina

o

Beyond the end of spinal cord extends a bundle of nerve roots

Arrangement of spinal cord is significant because there is little risk of

damaging the cord when a needle is inserted into the SA space below

the 1st lumbar level (usually space bet. L3-L4) to obtain a sample of CSF

Consists of nerve fibers / tracts :

White matter

o Surrounding an internal butterfly-shaped core of gray matter

or nerve cell bodieso Composed of afferent (sensory) and efferent (motor) fibers

that are organized into tracts and communicating fibers that

run bet the 2 sides of spinal cordo Each tract is assigned a unique position in the white matter

o Ascending tracts- conduct sensations w/c are relayed from spinal nerves and

receptors on opposite side of body to thalamus

o

Descending tracts- 2 types : pyramidal /corticospinal tracts and extrapyramidal

tractso

Pyramidal tracts

- conduct impulses concerned with voluntary movement from

motor cortex (upper motor neurons) to lower motor neurons inanterior horn @ app level of spinal cord

- most of these tracts cross in medulla

o

Extrapyramidal tracts

- carry impulses that modify and coordinate voluntary

movement and maintain posture Gray matter

o Anterior horns- consist of cell bodies of motor neurons whose axons leave the

spinal cord through the ventral root of spinal nerves to

innervate skeletal muscles

o

Posterior horns

- contain association (interneuron) neurons

II. Spinal Nerves

31 pairs of spinal nerves emerge from spinal cord carrying motor and

sensory fibers to and from organs and tissues of body

Named by loc in the vertebral column where they emerge and are

numbered within each section (eg. C1-C8) Each is connected to the spinal cord by two short roots

o Ventral /anterior root - made up of efferent or motor fibers from lower motorneurons in anterior horn

o Dorsal/ posterior root

- made up of afferent or sensory fibers from dorsal root

ganglion (collection of nerve cell bodies) where sensory fibersfrom peripheral receptors have already synapsed

Dermatome o Area of sensory innervations of skin by a specific spinal nerve

o Can be drawn on a “map” of the body surface

o

Assessment of sensory awareness using dermatome map can be

essential to determine level of damage to spinal cord

Plexuses

o

Four :

- cervical- brachial

- lumbar

- sacral

o Fibers from several spinal nerves branch and then re-form in

diff combinations to become specific peripheral nerves

o Phrenic nerve- consists of fibers from spinal nerves C3-C5

o Sciatic nerve

- contains fibers from spinal nerves L4-L5 and S1-S3o

The dispersal pattern can minimize the effects on a muscle’s

contraction of damage to one spinal cord segment

III. Reflexes

Automatic , rapid, involuntary responses to a stimulus

Involves a sensory stimulus from a receptor that is conducted along an

afferent nerve fiber , a synapse in spinal cord and an efferent impulsethat is conducted along a peripheral nerve to elicit a response

Acquired /learned reflexes such as those developed when learning toride a bicycle

Patellar/knee-jerk reflex or oculocephalic (doll’s head eye response)

reflex are useful in diagnosis

Absent, weak or abnormal responses may indicate presence of

neurologic problem and sometimes can show location of spinal cord

damage



Neurons and Conduction of Impulses

I. Neurons

Neurons / nerve cells

Highly specialized, nonmitotic cells that conduct impulses throughout

CNS and PNS

Require glucose and O2 for metabolism

Dendrite

o Receptor siteo

Conduct impulses toward the cellbody

Cellbodyo

Contains the nucleus

Axon

o Conducts impulses away from cellbody toward an effector site

or connecting neuron where it can release neurotransmitter

chemicals @ its terminal point

Myelin sheath

o Insulates the fiber and speeds up the rate of conduction

o Formed by schwann cellso Nucleus and cytoplasm of schwann cell form the neurilemma or

sheath of schwann, around the myelin

Nodes of Ranvier

o Axon collateral branches may emerge and stimuli may affect

the axon

Glial (neuroglial) cells

o Support and protect the neurons

o

Astroglia /Astrocytes- provide a link bet neurons and capillaries for physical and

prolly metabolic support as well as contributing to the blood-brain barrier

o Oligodendroglia

- provide myelin for axons in the CNSo Microglia

- Have phagocytic activity

o

Ependymal cells

- line the ventricles and neural tube cavity

- form the part of choroid plexus

Regeneration of neurons

Neurons cannot undergo cell division

If the cellbody is damaged, neuron dies In PNS, axon may be able to regenerate if cellbody is viable

After damage to the axon occurs :

o The section distal to injury degenerates because it lacksnutrients and is removed by macrophages and schwann cells

o Schwann cells then attempt to form a new tube @ the end of

remaining axono

Cellbody becomes larger and synthesizes addt'l proteins for

the growth of replacement axon

o

The new growth does not always occur appropriately or make

its original connections, because the surrounding tissue may

interfere

II. Conduction of Impulses

Depolarization

A stimulus increases permeability of neuronal membrane allowing Naions to flow inside cell thus depolarizing it and generating an action

potential The change to a + electrical charge inside the membrane results in

increased permeability of adjacent area and the impulse moves along

the membrane

Decrease in electrical charge across a membrane due to inward flow

of Na ions

Repolarization / Recovery

Reestablishment of the resting membrane potential after

depolarization occurred

Potassium ions move outward

Normal permeability of membrane is restored Sodium-Potassium pump :

o System of coupled ion pumps that actively tranports Na ionsout of a cell and K ions into cell @the same time

o Returns the Na and K ions to their normal locations

Saltatory conduction

Propagation of an action potential (nerve impulse) along the exposed

portions of a myelinated nerve fiber action potential appears @ successive nodes of Ranvier and therefore

seems to jump or leap from node to node

Synapase

Provides connection bet :o 2 or more neurons

o neuron and an effector site

EEG/ encephalogram

Measure brainwaves

III. Synapses and Chemical Neurotransmitters

Typical synapse consists of :- Terminal axon of presynaptic neuron

- Vesicles in terminal axon with neurotransmitter

- Receptor site on membrane of postsynaptic neuron - Axon and Receptor site are separated by fluid-filled synaptic cleft

Neurotransmitters (few examples) :1. Acetylcholine (ACh)

- Present @ neuromuscular junctions and in ANS, PNS and less commonly in

CNS

2. Catecholamines- Norepinephrine (SNS) ,Epinephrine, Dopamine

3. Serotonin4. Histamine

5. Gamma-aminobutyric acid (GABA)



Stimulus reaches the axon

Neurotransmitter flowsacross the synaptic cleft

Neurotransmitter is releasedfrom vesicles

Neurotransmitter act on

receptor in postsynaptic

membrane

Stimulus / Response

Inactivated by enzymesTaken up by presynaptic axon

to prevent continuedstimulation



Autonomic Nervous system

Incorporates the Sympathetic and Parasympathetic NS

Generally have antagonistic effects thereby providing a fine balance

that aids in maintain homeostasis in body Provides motor and sensory innervations to smooth muscle, cardiac

muscle and glands

Although individual is largely unaware of the involuntary activity , it is

integrated with somatic activity by the higher brain centers

Neural pathways in motor fibers of ANS differ from somatic nerves

because each involves 2 neurons and a gangliono

Preganglionic fiber is located in brain and spinal cordo Axon then synapses within the second neuron in the ganglion

outside CNS

o Postganglionic fiber continues to the effector organ or

tissue

I. Sympathetic NS

Thoracolumbar NS Increases the general level of activity in the body

Necessary for fight-or-flight or stress response

Augmented by the increased secretions of adrenal medulla in response

to SNS stimuli

Preganglionic fibers

o Arise from the thoracic and the 2 lumbar segments of thespinal cord

Gangliao

Located in 2 chains or trunks , one on either side of spinal cord

o Preganglionic fibers synapse with postganglionic fibers or

connecting fibers to other ganglia in the chain

Neurotransmitters and Receptors

o Important in ANS because they are closely linked to drug

actionso Cholinergic fibers / Acetylcholine

- the neurotransmitter released by preganglionic fibers at theganglion

- the postganglionic fibers to sweat glands and blood vessels in

skeletal muscle

o

Adrenaline fibers/ norepinephrine

- released by most SNS postganglionic fibers

Adrenergic receptors :

o Norepinephrine

- acts primarily on alpha receptorso

Epinephrine

- acts on both alpha and beta receptors

o

An organ or tissue may have more than 1 type of receptor but

one type is usually present in greater numbers and exerts

dominant effecto Drugs may be used to stimulate receptors or to prevent

stimulation :- beta adrenergic blocking agents (beta blockers) may be used

to block beta receptors

- beta adrenergic drug to stimulate beta receptors- the best drugs are specific for 1 type of receptor in one

organ or tissue and do not alter function in other areas of the

body- the more specific the drug action is the milder the adverse

effects of the drug

II. Parasympathetic NS

Craniosacral NS

Dominates the digestive system

Aids in the recovery of the body after sympathetic activity

2 locations of PNS Preganglionic fibers :

o Cranial nerves III, VII, IX, and X @ the brainstem level

o

Sacral spinal nerves

Vagus nerve :

o

Provides extensive innervations to the heart and digestivetract

Ganglia are scattered and located close to the target organ

Neurotransmitter @ both Preganglionic and postganglionic synapses is

Ach

2 types of cholinergic receptors :

o Nicotinic receptors

- always stimulated by Ach

- located in all postganglionic cholinergic neurons in the PNS

and SNS

o

Muscarinic receptors

- located in all effector cells

- may be stimulated or inhibited by ACh depending on theorgan

Cholinergic blocking agents

o Reduce PNS activity

Cholinergic / Anticholinesterase agentso Prevent the enzyme cholinesterase from breaking down Ach

o Increases PNS activity



General Effects of Neurologic Dysfunction

Local (Focal) effects

Signs r/t the specific area of the brain or spinal cord w/c the lesion

is located

o Paralysis of R arm that results from damage to a section of Lfrontal lobe

o Loss of vision that results from damage to the occipital lobe

o With an expanding lesion (eg. growing tumor/ hemorrhage) ,addt’l impairment is noted as the adjacent areas become

involved

Supratentorial and Infratentorial Lesions

Supratentorial Lesion Occur in cerebral hemispheres above tentorium cerebelli Leads to a specific dysfunction in a discrete area, perhaps numbness

in a hand

Must become very large before it affects consciousness

Infratentorial Lesion

Located in the brainstem / below tentorium May affect motor and sensory fibers resulting in widespread

impairment because nerves are bundled together when passing

through the brainstem

Resp and circulatory function and LOC may also be impaired

L and R hemispheres

L sided brain damage impairs :

Logical thinking ability Analytical skills

Intellectual abilities Communication skills

R sided brain damage impairs :

Appreciation of music and art

Behavior

Spatial orientation

Recognition of relationships

LOC Cerebral cortex and RAS in brainstem determine the LOC

Information must be processed in the association areas of cortex

before one is conscious of the info

Extensive Supratentorial lesions must be present in the cerebral

hemisphere to cause loss of consciousness Relatively small lesions in the brainstem / Infratentorial lesions can

affect the RAS The ff can also cause reduced LOC :

o

Space-occupying masses in cerebellum can also compress

brainstem and RAS

o

Systemic disorders (eg. acidosis / hypoglycemia) can depress

CNS

Various levels of reduced consciousness may present as :

o

Lethargy

o

Confusiono Disorientationo

Memory loss

o Unresponsiveness to verbal stimuli

o

Difficulty of arousal

Coma

o Most serious level of loss of consciousnesso

Affected person does not respond to painful or verbal stimuli

o Body is flaccid although some reflexes are present

Deep coma

o Terminal stage

o Loss of all reflexeso

Fixed and dilated pupils

o Slow and irregular pulse and resp

Vegetative state

o Loss of awareness and mental capabilities resulting fromdiffuse brain damage

o Appears to be a sleep-wake cycle (eyes are open or closed)

but person is unresponsive to stimulio

Some may in time recover consciousness but often survive

with significant neurologic impairment

Locked-in syndrome

o Person with brain damage is aware and capable of thinking

but is paralyzed and cannot communicate

o

Some can move their eyes in a “yes” or “no response

Brain death (criteria)

o

Cessation of brain function (eg. a flat or inactive EEG)o Absence of brainstem reflexes

o Absence of spontaneous respirations when ventilatorassistance is withdrawn

o Establishment of the certainty of irreversible brain damage

by confirmation of the cause of dysfunction

Drug overdose or hypothermia can cause loss of brain activitytemporarily thus a longer time period and addt’l testing are required

before brain death can be confirmed in this case

Motor dysfunction Damage to the upper motor neurons:

o In the cerebral cortex (frontal lobe) or to the corticospinal

tracts in brain

o

Interferes with voluntary movements causing weakness or

paralysis on the opposite (contralateral) side of the body

The contralateral effect is determined by the crossover of thecorticospinal tracts in the medulla

Hyperreflexia

o

Muscle tone and reflexes may be increased because the

intact spinal cord continues to conduct impulses with no

moderating or inhibiting influences sent from brain (spasticparalysis)

o Frequently leads to contractures in the affected limbs

-- Damage to the lower motor neurons :

o In the anterior horns of the spinal cord

o Causes weakness or paralysis on the same side of the bodyand below level of damage

In the area of damage :

o Muscles are usually flaccid (lack tone)

o

Reflexes are absent (flaccid paralysis) If the cord distal to the damage is intact , some reflexes in that area

may be present and hyperactive (hyperreflexia)

Lower motor neurons are also located in nuclei of cranial nerves in

brainstem :o

Ipsilateral weakness (same side) or flaccid paralysis may

result from damage to any cranial nerves containing motor

fibers

--

Two involuntary motor responses that occur in persons with severe brain

trauma : Decorticate posturing

o

Rigid flexion in the upper limbs

o Adducted arms and internal rotation of hands

o Lower limbs are extended

o

May occur in persons with severe damage in cerebralhemispheres

Decerebrate posturing

o Occur in persons with brainstem lesions and CNS depression

caused by systemic effects

o

Both the upper and lower limbs are extended

Sensory deficits May involve :

o

Touch

o Pain

o Tempo

Position

o Special senses of vision, hearing , taste and smell

Somatosensory cortex in parietal lobe



o Recieves and localizes basic sensory input from body

o

Mapped to correspond to receptors in skin and skeletal

muscles of various body regions

o Specific site of damage determines deficit

Dermatomes

o Mapping assists in evaluation of spinal cord lesions

Visual Loss : Hemianopia

Loss of visual field depends on site of damage in visual pathway

@ the optic chiasm (crossover)

o

Fibers in each optic nerve come together and then divideo If optic chiasm is totally destroyed , vision is lost in both

eyes

Partial loss can result in variety of effects depending on particular

fibers damaged Fibers from medial (inner) half of each retina (cells receive visual

stimuli)

o Cross over to the other hemisphere

Fibers from lateral (outer) half of each retina

o Remain on the same side Optic tract coursing from optic chiasm to the occipital lobe on one

side includes fibers from half of each eye

Homonymous hemianopia

o

If optic tract or occipital lobe is damaged , vision is lost from

medial half of one eye and lateral half of other eye

o Overall effect is loss of visual field on the side opposite to

that of damage

o Damage to L occipital lobe = loss of R visual field- because L half of both retinas receives light waves from R

side of visual field

Language Disorders

Aphasia

o Inability to comprehend or to express languageo

Main types :

- expressive

- receptive

- global Expressive /motor aphasia

o

Impaired ability to speak or write fluently

o

Person may be unable to find any intelligible words orconstruct a meaningful senstence

o Occurs when Broca’s area in dominant frontal lobe (usually L

lobe) , inferior motor cortex is damaged

Receptive /sensory aphasia

o Inability to read or understand the spoken word

o Does not include hearing or visual impairment

o Source of problem is inability to process info in brain

o Person may be capable of fluent speech , but frequently it ismeaningless

o Damage to Wernicke’s area in L temporal lobe

Global aphasia

o Combination of expressive and receptive aphasia

o Results from major damage to the brain including Broca’s

area, Wernicke’s area and many communicating fibers

throughout brain

Other types

Dysarthria

o Words cannot be articulated clearlyo Motor dysfunction that usually results from cranial nerve

damage or muscle impairment

Agraphia

o Impaired writing ability

Alexia

o Impaired reading ability Agnosia

o Loss of recognition or association

o Visual Agnosia indicates inability to recognize objects

Seizures

Convulsions

Caused by spontaneous excessive discharge of neurons in the brain May be precipitated by :

o

Inflammation in brain

o Hypoxia “

o

Bleeding “

Can be focal or generalized Frequently manifested by involuntary repetitive movements or

abnormal sensations

Increased Intracranial Pressure

Definition

Any increase in fluid (blood / inflammatory exudate) or any addt’l

mass (tumor) causes an increase pressure in brain

Result is less arterial blood can enter the “high-pressure” area in

brain

Eventually brain tissue itself is compressed Effects decrease function of the neurons both locally and generally

and eventually brain tissue dies Pressure increases @ the site of problem initially but gradually is

dispersed throughout the CNS by means of continuous flow of CSF

and blood leading to widespread loss of function

Changes in ICP can be monitored by :

o

Instruments placed in ventricles (invasive procedure) (direct)o Methods such as radiologic examinations or assessment of

LOC and v/s (indirect) Common in many neurologic problems including :

o

Brain hemorrhage

o Trauma

o Cerebral edema

o Infection

o Tumorso

Accumulation of excessive amt of CSF

Early Signs

Compensation mechanisms when ICP increases :

o Body initially shifts more CSF to the spinal cavity

o

Increasing venous return from brain

o Resulting hypoxia triggers arterial vasodilation in the brain

through local autoregulatory reflexes in an attempt otimprove blood supply to brain but this adds to fluid volume

inside skull so it is effective for only a short time

Decreased LOC is the first indication of increased ICP

Addt’l early indications :

o Severe headache- occurs from stretching of dura and walls of large blood

vessels

o

Projectile Vomiting

- result of pressure stimulating the emetic center in medulla

o Papilledema- caused by increased ICP and swelling of the optic disc

- can be observed by looking through the pupil of the eye @the retina , where the optic disc provides a “window” into the

brain

- optic nerve (cranial nerve II) is a projection of brain tissue

that is surrounded by CSF and meninges and enters the eye@ the optic disc where it reflects the effects of increased

ICP of brain

Vital Signs

Cerebral ischemia develops

o Stimulates a powerful response (Cushing’s reflex) from the

vasomotor centers in an attempt to increase arterial bloodsupply to the brain

Systemic vasoconstriction occurs

o

Increase systemic BP

o Force more blood into the brain to relive ischemia Baroreceptors in carotid arteries

o Respond to the increased BP by slowing the HR Chemoreceptors



Acute Neurologic Problems

Brain tumors

I. Definition

Space-occupying lesions that cause increased ICP because of space

constraints within rigid skull

Benign or malignant tumors can be life-threatening unless they are in

an accessible superficial location where they can be removed

Gliomas

o

Form the largest category of primary malignant tumorso Arise from one of the glial cells , the parenchymal cells in CNS

o

Further classified acc to :

- cell of derivation (astrocytomas are most common)

- location of tumor May develop from meninges (meningioma) or pituitary gland (adenoma)

Primary malignant tumors

o

Rarely metastasize outside CNS

o Multiple tumors may be present within CNS Secondary brain tumors

o Quite common

o Usually metastasizing from breast or lung tumors

o Cause effects similar to those of primary brain tumors

Diagnosis is made by :

o MRIo

Stereotactic biopsy

II. Pathophysiology

Primary malignant tumors (particularly astrocytomas)

o

Do not usually have well-defined margins

o Invasive and have irregular projections into adjacent tissue

that are difficult to totally remove The ff increases ICP :

o Obstruction of CSF or of venous sinuseso

An area of inflammation around tumor

As the mass expands , it compresses and distorts the tissue around it

eventually resulting in herniation

III. Etiology

Brainstem and cerebellar tumors are common in young children

Tumor occur in adults most often in mid-life

Adults are affected more frequently by tumors in cerebral

hemispheres

IV. Signs and Symptoms

Specific site of tumor determines the focal signs If tumor grows rapidly, signs of increased ICP develop quickly , often

beginning with morning headaches ; overtime headaches increase in

severity and frequency Vomiting occurs

Lethargy and irritability may develop along with behavioral changes

In some cases, focal or generalized seizures are the first sign, as the

tumor irritates surrounding tissue Brainstem or cerebellar tumors may affect several cranial nerves

possibly causing unilateral facial paralysis or visual problems

Brain tumors unlike other forms of cancer do not cause the usual

systemic signs of malignancy because they do not metastasize outside

CNS and they will cause death before they are large enough to cause

gen effects Pituitary adenomas in brain usually cause endocrinologic signs

depending on type of excess secretion

Visual disturbances resulting from compression of adjacent optic

chiasm , nerves or tract Headaches and visual signs may result from increased ICP

V. Treatment

Surgery is the treatment of choice if tumor is reasonably accessible

Chemotherapy is often accompanied by radiation

In some cases, surgery and radiation may cause substantial damage to

normal tissue in CNS



Vascular Disorders (3)

Transient Ischemic Attack (TIAs)

I. Definition

Results from a temporary localized reduction of blood flow in the

brain

Recovery occurs within 24 h

II. Pathophysiology

May be caused by :

o

Partial occlusion of an artery caused by atherosclerosiso Small embolus

o

Vascular spasm

o Local loss of autoregulation Advantageous if it serve as a warning and lead to early diagnosis and

treatment of a problem before the occurrence of stroke

Brain must have a constant source of glucose and O2 or suffer

permanent damage

Not all strokes are preceded by TIAs

III. Signs and Symptoms

Directly r/t location of ischemia

Pt remains conscious The ff may occur :

o

Muscle weakness in an arm or leg

o

Visual disturbanceso

Numbness

o Paresthesia in face

o Transient aphasia

o

Confusion

Attack may last a few min or longer but rarely lasts > 1-2 h and then

signs disappear Repeated attacks are frequently a warning of the development of

obstruction r/t atherosclerosis



Cerebrovascular Accidents (CVA)

I. Pathophysiology

Development and effects of stroke vary with cause:

Occlusion of an artery by an atheroma

o Most common cause of CVA

o

Atheromas often develop in large arteries (eg. carotid

arteries)

o Causes gradual narrowing of arterial lumen by plaque and

thrombus

o Leads to possible TIAs and eventually infarction

Sudden obstruction caused by an embolus lodging in cerebral arteryo

Thrombi may break off of an atheroma or

o Mural thrombi may form inside the heart after a MI andthen break away

o Can also result from other materials : tumors, air , infection

(eg. endocarditis) Intracerebral hemorrhage / Hemorrhagic strokes

o Usually caused by rupture of a cerebral artery in pt withsevere HTN

o Frequently more severe and destructive than other CVAs

because they affect large portions of braino Because of the greater increase in ICP with hemorrhage,

effects are evident in both hemispheres and are

complicated by secondary effects of bleedingo Presence of free blood in interstitial areas affects the cell

membrane and can lead to secondary damage such as :- vasospasm

- electrolyte imbalances

- acidosis

- cellular edema

--

Five min (or less) of ischemia causes irreversible cell damage

Cerebral edema and an increasing area of infarction in first 48-72 h

tend to increase the neurologic deficits Inflammation and pressure in brain must be minimized as quickly as

possible and therapy instituted to dissolve thrombi and maintain

adequate perfusion adequate perfusion to limit area of permanent

damage Collateral circulation may have already developed in areas gradually

affected by atherosclerosis

Because neurons do not regenerate , an area of residual scar tissue

and often cysts remains, with a permanent loss of neurons in that area In many cases, because specific functions result from integrated

output from many areas, it is possible with intensive therapy for a

person who has experienced a stroke to develop new neural pathways

in brain or to relearn a task thus recovering some lost function

Complications are common :

o Recurrent CVA

o

Secondary problems r/t immobility : pneumonia, aspiration,

constipationo Contractures r/t paralysis

II. Etiology

Risk factors :

o DM

o HTN

o Systemic lupus erythematosuso

Elevated cholesterol levels

o Hyperlipidemia

o

Atherosclerosis

o History of TIAs

o Increasing age

o

Heart disease

Combination of oral conctraceptives and cigarette smoking has beenwell documented as an etiologic factor

Emboli may arise from ;

o Atheromas in large arteries (eg. carotid)

o

Cardiac disorders of L ventricle (eg. MI, atrial fibrillation,

endocarditis)

o Implant (eg. prosthetic valve)

Risk of intracerebral hemorrhage increase in :

o Pt with long term HTN

o

Pt with arteriosclerosis

Total occlusion of a cerebral

blood vessel by atheroma orembolus

Lack of blood inbrain tissue

Rupturedcerebral vessel

Tissue

necrosis/Infarction

Central area of necrosis developssurrounded by an area of inflammation

and function in the area is lost

immediately

Tissue liquefies

Cavity in brain




Depend on :

o Location of obstructiono

Size of artery involved

o Functional area affected

Presence of collateral circulation may diminish the size of affected

area Silent areas of brain

o

In w/c dysfunction resulting from small infarctions is not

obvious

Obstruction of small arteries may not lead to obvious signs untilseveral small infarctions have occurred

Evolving stroke

o

Effects of a stroke develop slowly over a period of hours

Initially flaccid paralysis is present

Spastic paralysis develops several weeks later as NS recovers from

initial insult Generally , functional deficits increase the first 48 h as inflammation

develops @ the site and then subside as some neurons around

infracted area recover

Occlusion of large arteries / hemorrhage may cause :

o

Coma

o Loss of consciousness

o

Death almost immediately

Hemorrhagic strokes usually begin suddenly with a blinding headache

and increasingly severe neurologic deficits

Specific local signso Depend on area affected (eg. occlusion of an anterior

cerebral artery affects frontal lobe)

o Common signs :

- contralateral muscle weakness / paralysis- sensory loss in leg

- confusion- loss of problem-solving skills

- personality changes Middle cerebral artery

o Supplies a large portion of cerebral hemisphere

o Lack of blood supply to this artery leads to contralateral

paralysis and sensory loss primarily of upper body and arm

Aphasia occurs when dominant hemispheres of brain is affected Spatial relationships may be more severely impaired if R side is

damaged

Posterior cerebral arteryo Supplies the occipital lobeo Visual loss is likely if it is occluded

IV. Treatment

“Clot-busting agents” eg. Tissue plasminogen activator (tPA)

Surgical interventions – to relieve carotid artery obstruction Glucocorticoids – may reduce cerebral edema

O2 supply – to maximize cerebral circulation

Assisting pt’s return to a sitting or standing passion as soon as v/s are

stable – to maintain muscle tone and minimize perceptual deficits

Correct positioning , frequent changes of position, and passive

exercises – to prevent muscle atrophy, contractures and skin

breakdown

Cerebral Aneurysms

I. Pathophysiology An aneurysm is a localized dilation in an artery

Frequently multiple

Usually occur @ the points of bifurcation on the circle of Willis Develop where there is a weakness in the arterial wall where

branching occurs

Force of blood leads to bulging in the wall, w/c is often aggravated by

HPN

Initially, are small and asymptomatic

Tend to enlarge over years until compression of the nearby structures

(eg. a cranial nerve) causes clinical signs or rupture occurs Rupture

o Often results from a sudden increase in BP during exertion

o

Bleeding occurs into the SA space (location of circle of Willis)

and CSF

o May be a small leak or a massive tearo

Blood is irritating to the meninges and causes an inflammatory

response and irritation of the nerve roots passing through

the meningeso The free blood also causes vasospasm in cerebral arteries,

further reducing perfusion and leading to addt’l ischemia

o

Hemorrhage from ruptured vessels causes increased ICP and

its associated signs

o

No focal signs are present because addt’l blood is dispersedthrough the system

o SA hemorrhages may be classified acc.to their clinicaleffects

II. Signs and Symptoms

Enlarging aneurysm :

May cause pressure on surrounding structures

Small leak :

Headache as tension increases on blood vessel wall and meninges

Photophobia

Intermittent periods of dysfunction :

o Confusion

o Slurred speech

o

Weakness Nuchal rigidity

o A stiff, extended neck

o Often develops because the escaped blood irritates the spina

nerve roots and causes muscle contractions in neck

Massive rupture/ SA hemorrhage :

Immediate, severe , “blinding” headache

Vomiting Photophobia

Seizures Loss of consciousness

Death may occur shortly after rupture

III. Treatment

Before rupture : Can be treated surgically ASAP by clipping or trying it off

While pt is waiting for surgery, sudden increases in BP must be

prevented

After rupture : Surgical clipping may also be done

There is substantial risk of rebleeding @ the site of repair or from

other aneurysms

Addt’l therapeutic measures focus on reducing effects of :

Increased ICP

Cerebral vasospasm



Infections (5)

Meningitis

I. Definition

An infection , usually bacterial , of the meninges of CNS

Many microbes can infect CNS

All age groups are susceptible

II. Pathophysiology

Microorganisms reach the brain :

o

Via blood

o By extension from nearby tissue

o By direct access through wounds

Meningococcus

o Can bind to nasopharyngeal cells in an individualo

Cross mucosal barrier , attach to the choroid plexus and

enter CSF Infection spreads rapidly through coverings of brain because :

o Membranes are continuous around CNS

o CSF flows in SA space Focal signs are absent because there is no localized mass of infection

Inflammatory response to infection leads to :

o Increased ICPo

Pia and Arachnoid layers become edematous

Common bacterial infections lead to :o

Purulent exudate that covers surface of brain and fills the

sulci, causing surface to appear flat

o Exudate is present in CSF

o

Blood vessels on surface of brain appear dilated

III. Etiology

In some categories, vaccines have reduced the risk

Diff. age groups are susceptible to diff. organisms that cause meningitis

Neisseria meningitidis / meningococcus

o

Classic meningitis pathogen in children and young adults

o Frequently carried in nasopharynx of asymptomatic carriers

o

Spread by resp. droplets

o Any close contacts of affected persons should be given

prophylactic treatmento

Epidemics are common in schools or institutions where close

contact bet. children is likely to spread the organism

Escherichia coli

o Most common causative organism in neonates

o Usually seen in conjunction with :- a neural tube defect

- premature rupture of amniotic membranes- a difficult delivery

Haemophilus influenza

o Meningitis results most often from bacterial infections in young children

Streptococcus pneumoniae

o Major cause of meningitis in elderly persons and youngchildren

Other cause :

S/t other infections (sinusitis, otitis) Abscess located where the infection can spread through bone to

meninges (eg. an abscessed tooth) Any form of head trauma or surgery from a variety of microorganisms

Aseptic /viral meningitis Results from an infection (eg. mumps, measles)


Sudden onset of meningitis is common

Meningeal irritation leads to :

Severe headache

Back pain Photophobia

Nuchal rigidity (hyperextended , stiff neck)

2 other clinical signs of meningeal irritation Kernig’s sign

o Resistance to leg extension when lying with hip flexed

Brudzinski’s sign

o Neck flexion causes flexion of hip and knee

Early indicators of increased ICP

Vomiting

Irritability

Lethargy

Stupor

Seizures

Indicators of infection Fever

Chills

Leukocytosis (increased WBC production)

Meningococcal infections

Petechial rash

Extensive ecchymoses over body

Potential complications : Hydrocephalus

o If CSF flow is blocked by pus or adhesions Cranial nerve damage

Damage to cerebral cortex resulting in :

o Mental retardation

o

Seizures

o Motor impairment

In fulminant (rapidly progressive, severe) cases caused by highly virulent

organisms (frequently meningococcal) Disseminated intravascular coagulation develops with associated

hemorrhage of adrenal glands or meningococcal septicemia may

directly cause adrenal hemorrhage (Waterhouse-Friderichsensyndrome)

Usually result in vascular collapse or shock and death

V. Diagnostic tests

Examination of CSF obtained by lumbar puncture , confirms the

diagnosis If present :

o CSF pressure is elevated

o CSF will appear cloudyo

CSF usually contains an increased # of leukocytes

Causative organism in CSF or blood must be identified to ensure

effective treatment

VI. Treatment

Aggressive antimicrobial therapy (eg. ampicillin) Specific treatment measures for ICP and seizures

Glucocorticoids reduce cerebral inflammation and edema

Vaccines are available as a preventive measure

Carriers should be identified in institutional epidemics

VII. Prognosis

With prompt dx and treatment , majority of pt survive

Mortality rate in neonatal meningitis is high

There is some risk of permanent brain damage in young children



Brain Abscess

A localized infection , frequently occurring in frontal or temporal

lobes There is usually necrosis of brain tissue and a surrounding area of

edema Usually result from :

o

Spread of organisms from ear, throat, lung or sinus

infection

o Multiple septic emboli from acute bacterial endocarditiso

Directly from a site of injury or surgery

Common organisms :o

Staphylococci

o Streptococci

o Pneumococci

Onset tends to be insidious Focal signs indicating neurologic deficits and increasing ICP develop

The ff are required :

o Surgical drainage

o Antimicrobial therapy

Mortality rate : 10 %

Encephalitis

An infection of the parenchymal or connective tissue in the brain and

cord (particularly basal ganglia)

May include the meninges

Necrosis and inflammation develop in brain tissue, often resulting in

some permanent damage

Early signs of infection :

o Severe headacheo

Stiff neck

o Lethargy

o

Vomiting

o Seizures

o Fever

Usually of viral origin but may be r/t other organisms

I. Western equine encephalitis

An arboviral infection spread by mosquitoes

Occurs more frequently in summer months

Common in young children

II. St. Louis encephalitis Affects older persons more seriously than younger ones

III. West Nile fever

Originated in northeastern US

Caused by a flavivirus, spread by mosquitoes w/ certain birds as an

intermediate host

Focus for control has been to track the spread and reduce risk of

mosquito bites in affected areas Initally causes flu-like sx w/ low grade fever and headache , sometimes

followed by confusion and tremors

IV. Neuroborreliosis (Lyme disease)

Caused by a spirochete, Borrelia burgdorferi , transmitted by tick

bites in summertime Site of tick bite :

o Redo With a pale center

o Gradually increasing in size to form the unique marker lesion,a “bull’s eye”

Microbes disseminate through circulation , causing :

First :o Sore throat

o Dry cougho

Fever

o Headache

Followed by :

o Cardiac arrhythmias

o Neurologic abnormalities (eg. facial nerve paralysis) r/tmeningoencephalitis

Lastly ..

o Pain and Swelling may develop in large jointso

Sometimes progressing to chronic arthritis

Prolonged therapy w/ antimicrobials such as doxycycline is prescribed

V. Herpes simplex encephalitis Occurs occasionally and is dangerous

Arising from spread of herpes simplex virus type 1 (HSV-1) from the

trigeminal nerve ganglion

The virus causes extensive necrosis and hemorrhage in brain , ofteninvolving frontal and temporal lobes

Early treatment w/ an antiviral drug such as acyclovir may control

infection ; otherwise treatment is supportive

Other Infections

Rabies (hydrophobia) Caused by a virus that is transmitted by the bite of a rabid animal Virus travels along peripheral nerves to the CNS , where it causes

severe inflammation and necrosis, particularly in the brainstem and

basal ganglia Incubation period :

o Often 1-3 months

o Depends on the distance bet. the bite and access to the CNS

Onset is marked by :

o

Headacheo

Fever

o Nervous hyperirritability

o Sensitivity to touch

o

Seizures

Virus also travels to salivary glands Difficulty swallowing caused by muscle spasm and foaming @ the mouth

are typical

Resp.failure causes death

Necessary treatments :

o Immediate cleansing of bite area

o

Prophylactic immunization

Tetanus (lockjaw) Caused by Clostridium tetani, a spore-forming bacillus Spores survive for years in soil

The vegetative form is an Anaerobe , thriving deep in tissues ,for ex. in

a puncture wound

Exotoxin enters the NS , causing tonic muscle spasms

Sx :

o Jaw stiffnesso

Difficulty swallowing

o Stiff neck

o

Headache

o Skeletal muscle spasm

o Eventually ..resp. failure

Mortality rate is 50 % Immunizations are advised w/ boosters as needed or ff injury

Poliomyelitis (infantile paralysis)

Polio viruso

Highly contagious through direct contact or oral doplet

o Reproduces in lymphoid tissue in oropharynx and digestive

tract , then enters blood and eventually CNSo Attacks the motor neurons of the spinal cord and medulla ,

causing minor flulike effects in many cases, but paralysis andresp. failure in other cases , depending on level of destruction

Sx :

o

Fever

o Headache

o Vomiting

o Stiff neck

o Pain

o

Flaccid paralysis



Postpolio syndrome (PPS)

Has been occurring 10-40 years after recovery from the original

infection w/ progressive and debilitating fatigue, weakness , pain and

muscle atrophy

Infection-Related Syndromes

Reye’s syndrome

I. Pathophysiology Unknown cause but is linked to a viral infection such as influenza in

young children that have been treated with aspirin (ASA)

Depending on particular virus, signs appear 3-5 days after the onset

of viral infection Acetaminophen is now used to treat fever in children Major pathologic changes occur in the brain and liver

o

A noninflammatory cerebral edema develops leading to

increased ICP

o Brain function is severely impaired by cerebral edema and

effects of high ammonia levels in serum r/t liver dysfunction

o Liver enlarges, develops fatty changes in the tissue and

progresses to acute failureo Jaundice is not present, but serum levels of liver enzymes are

elevatedo

Resultant metabolic abnormalities : hypoglycemia and

increased lactic acid in blood and body fluids w/c also

contribute to acute encephalopathy

II. Signs and Symptoms

Vary in severity

Encephalopathy initially causes :

o Lethargy

o Headacheo

Vomiting

w/c are quickly followed by :

o disorientation

o Hyperreflexia

o Hyperventilation

o

Seizures

o

Stuporo Coma

III. Treatment

No immediate cure Treatment is supportive and symptomatic , managing the metabolic

imbalances and cerebral edema

Guillain-Bare syndrome

I. Definition

Also known as :

o

Post-infectious polyneuritis

o Acute idiopathic polyneuropathy

o

Acute infectious polyradiculoneuritis An inflammatory condition of the PNS

II. Pathophysiology

Cause is unknown

Evidence indicates that an abnormal immune response, perhaps an

autoimmune response , precipitated by a preceding viral infection orimmunization may be responsible

Local inflammation accompanied by :

o

Accumulated lymphocytes

o Demyelination

o Axon destruction

The above changes cause impaired nerve conduction particularly in

efferent (motor) fibers although afferent (sensory) and autonomic

fibers may also be involved If the cell body remains alive through the acute period, the axon can

regenerate

Initially, the inflammatory and degenerative processes affect the

peripheral nerves in legs ; then the inflammation ascends to involvethe spinal nerves to the trunk and neck and frequently includes cranial

nerves as well

Critical period :

o Ascending paralysis involves the diaphragm and respiratory

muscles Recovery :

o Usually spontaneous with the manifestations diminishing inreverse order i.e motor function is regained first in the

upper body and then gradually improves in trunk and lower

extremities


Progressive muscle weakness and areflexia beginning in the legs lead

to an ascending flaccid paralysis w/c may be accompanied by

Paresthesia or pain and gen muscle aching

As paralysis advances upward, vision and speech may be impaired

If swallowing and resp are affected , a life-threatening situation

develops

Many pt sustain ANS impairment manifested as :

o

Cardiac arrhythmiaso Labile (fluctuating) BP

o Loss of sweating capability

IV. Treatment

Treatment is primarily supportive

Ventilator is required in many cases

Use of immunoglobulin therapy or plasmapheresis in w/c IgG isseparated and removed from pt’s blood in early stage may shorten the

acute period of disease in some pt and hasten recovery Physiotherapy throughout recovery period is essential to maximize

restoration of function

About 30 % of pt exp residual weakness



Head Injuries

I. Definition

May involve :

o Skull fractures

o Hemorrhageo

Edema

o Direct injury to brain tissue

Can be :

o Mild – causing only bruising of tissue

o Severe – causing destruction of brain tissue and massive

swelling of brain Skull can also destroy brain by means of :

o

Bone fragments that penetrate or compress the brain tissue

o Inability of skull to expand to relieve pressure

II. Types

Concussion

Reversible interference with brain function Usually resulting from a mild blow to the head w/c causes sudden

excessive movement of brain , disrupting neurologic function and

leading to loss of consciousness Amnesia / memory loss and headaches may follow a concussion

Recovery with no permanent damage usually occurs within 24 h

Contusion

Bruising of brain tissue with rupture of small blood vessels and edema

Usually results from a blunt blow to the head

Possibility of residual damage depends on force of blow and degree of

tissue injury

Closed head injury

Skull is not fractured but brain tissue is injured and blood vessels

may be ruptured by force exerted against skull

Extensive damage may occur when head is rotated with considerable

force

Open head injury

Fractures or penetration of brain by missiles or sharp objects

Linear fractures

Simple cracks in the bone

Comminuted fractures

Several fracture lines but may not be complicated

Compound fractures

Trauma in w/c brain tissue is exposed to environment

Likely to be severely damaged because bone fragments may penetrate

the tissue

Risk of infection is high

Depressed skull fractures

Displacement of a piece of bone below the level of the skull thereby

compressing the brain tissue Blood supply to the area is often impaired

Considerable pressure is exerted on the brain

Basilar fractures

Occur @ the base of the skull Often accompanied by leaking of CSF through ears / nose

May occur when forehead hits a car windshield with considerable

force

Cranial nerve damage and dark discoloration around eyes are common

Contrecoup injury

Area of brain contralateral to the site of direct damage is injured as

brain bounces off the skul

May be secondary to acceleration or deceleration injuries

Skull and brain hit a solid object w/c causes brain to rebound against

opposite side of skull usually causing minor damage

III. Pathophysiology

Primary brain injuries

Direct injuries

May involve laceration or compression of brain tissue by :

o Piece of bone or foreign object

o Rupture or compression of the cerebral blood vessels Because brain is not held tightly in place :

o Application of unusual force may rotate or shift it inside the

skull

o Brain tissue may be damaged by the rough and irregular inner

surface of the skullo It may also be damaged by movement of lobes of brain against

each other (shearing injury)

Any trauma to the brain tissue causes loss of function in the part of

the body controlled by that specific area of brain

Cell damage and bleeding :

o Lead to inflammation and vasospasm around site of injury

increasing ICP and creating further gen ischemia and

dysfunction

o After bleeding and inflammation subside, some recovery ofneurons in the area surrounding direct damage may occur

o

Central area of damage undergoes necrosis and is replaced by

scar tissue or a cyst

Secondary brain injuries

Result from addt’l effects of :

o

Cerebral edemao Hemorrhage

o Hematoma

o Cerebral vasospasm

o Infectiono

Ischemia r/t systemic factors

Hematoma (Classification in relation to meninges)

Epidural (extradural) hematoma o Bleeding bet dura and skull

o Usually caused by tearing of middle meningeal artery in

temporal lobe

o Signs of trouble usually arise within a few h of injury when

person loses consciousness after a brief period of

responsiveness

Subdural hematoma o

Bleeding bet dura and arachnoido Frequently , there is small tear in a vein w/c causes blood to

accumulate slowly

o May be acute (signs present in 24 h) or subacute (increasing

ICP develops over a week or so)

o Chronic subdural hematoma may occur in an elderly person , in

whom brain atrophy allows more space for a hematoma to

develop

o A tear in the arachnoid can allow CSF to leak to into subduralspace (hygroma) creating addt’l pressure

Subarachnoid hemorrhage

o

Bleeding bet arachnoid and pia

o Associated with traumatic bleeding from blood vessels @ the

base of brain

o

Because blood mixes with circulating CSF , a localized

hematoma cannot form

Intracerebral hematoma

o

Results from contusions or shearing injuries

o May develop several days after injury

In all types of hematomas bleeding leads to :

o Local pressure on adjacent tissue

o General increase in ICP

Blood may be partially coagulated, forming a solid mass

When blood accumulates slowly :

o

Blood cells undergo hemolysis

o Fluid in area of cell breakdown exerts osmotic pressure ,

drawing more and more H2O into the area, increasing size andpressure of mass and raising ICP

Herniation may result from untreated mass



Any bleeding in brain may precipitate cerebral

vasoconstriction/vasospasm leading to further ischemia and more

damage to neurons

IV. Etiology

Sports injuries

Vehicular accidents Excessive alcohol intake

o

High blood alcohol level can impede neurologic assessment by

masking signs of injury

o

Alcohol, because of its dehydrating effects , tends to delayonset of cerebral edema and elevation of ICP but there may be

a greater increase in ICP @ a later time

Falls

o Common cause of head injury

o

More often in elderly persons

Boxers and other athletes

o At risk for repeated head injury

Infants

o When violently shaken, can experience severe damage to thebrain and brainstem as the head swings

Objects that fall on head

Blow to he head

V. Signs and Symptoms

Seizureso Often focal but may be generalized

o Due to irritating quality of blood

o Common sequelae after recovery because of increased

irritability of tissue around the scar

Cranial nerve impairment

o Particularly in persons who have sustained basilar fractures

Otorrhea / Rhinorrhea

o Occurs with fracture and tearing of the meninges w/c allows

fluid to pass out of SA space

o Provides microbes with an entry point into the brain Otorrhagia

o Blood leaking from ear through a fracture site with torn vessel

and meninges Fever

o

May be a sign of hypothalamic impairment or of cranial or

systemic infection Stress ulcers

o May develop from increased gastric secretions The ff are present for some time after recovery :

o

Gen fatigue

o Frequent headaches

o Memory loss

Complications of immobility

o Pneumoniao

Decubitus ulcers

VI. Treatment

CT scan – determine extent of brain injury

Glucocorticoid – decrease edema

Antibiotic – reduce risk of infection Surgery – to reduce ICP

Blood products and O2 - to protect the remaining brain tissue

Awakening person periodically – to check LOC

Checking for reactive pupils

Watching for vomiting and any change in movement, sensation or

behavior



Spinal Cord injury

I. Definition

Usually results from fracture or dislocation of the vertebrae , w/c

compresses , stretches or tears spinal cord Supporting ligaments and intervertebral disc may be damaged also

Most injuries occur in areas of spine that provide more mobility but

less support i.e C1-C7 and T12-L2

Immediate appropriate immobilization is essential to prevent

secondary damage

Common types of injuries : Cervical spine injuries

o

May result from hyperextension (upward) or hyperflexion

(downward) of the neck with possible fracture

o Usually damage to the disc and ligaments occurso Leads to :

- dislocation- loss of alignment of the vertebrae

- compression or stretching of the spinal cord Dislocation of any vertebra

o May crush or compress the spinal cord and compromise blood

supply Compression fractures

o Cause injury to the spinal cord when great force is applied to

the top of skull or to feet and is transmitted up or down thespine

o

The ff events can cause this injury :- diving into an empty pool

- jumping from a height and landing on the feet

- object falling on a standing person’s head

o

The shattered bone is compressed and protrudes , exerting

pressure horizontally against the cord

o Sharp edges of bone fragments may lacerate or tear nervefibers and blood vessels

Penetration injuries

o

Due to stab or bullet wounds

Vertebral fractures classification :

Simple

o Single line break

Compression

o Crushed or shattered bone in multiple fragments

Wedgeo

Displaced angular section of bone

Dislocation

o

Vertebra forced out of its normal position

II. Pathophysiology

Damage to the spinal cord may be temporary or permanent

Nerves in the spinal cord do not regenerate Laceration of nerve tissue by bone fragments usually results in

permanent loss of conduction in the affected nerve tracts

Complete transection

o Severing or crushing of the cord

o Causes irreversible loss of all function @ and below level of

injury

Partial transection

o May allow recovery of some function Bruising

o Reversible damage when mild edema and minor bleeding

temporarily impair conduction of nerve impulses

Any compression of cord must relieved quickly to maintain adequate

blood supply Prolonged ischemia and necrosis lead to permanent damage

Bleeding and inflammation develop locally, creating addt’l pressure and

further interfering with blood flow

Edema and hemorrhage extend for several segments above and below

level of injury Damaged to tissues releases mediators w/c cause vasoconstriction

leading to addt’l local ischemia and possible necrosis

o Norepinephrine

o

Serotonin

o Histamine Destructive enzymes are released as well causing more inflammation

and necrosis

Initially, loss of function may appear to be extensive because of addt’

compression , but as edema subsides , there may be partial recoveryof function

Regular assessment of movement and sensory response using

dermatome map can determine degree of damage or recovery in

spinal cord

Injury in cervical region : o Inflammation may extend upward to the level of C3-C5 ,

interfering with phrenic nerve innervatio to the diaphragmo

Affect respiration

o Ventilatory assistance may be required

Spinal shock

o A period where conduction of impulses ceases in the nerve

tracts and in the gray matter

o

A form of neurogenic shock The ff determine the rate and degree of recovery

o

Extent of injury

o

Amount of resultant bleeding

o Need for surgical intervention

Recovery period :

o Inflammation gradually subsides , damaged tissue is removed

by phagocytes and scar tissue begins to form

o

Reflex activity resumes in spinal cord below level of injury o Any undamaged tracts continue to conduct impulses through

level of damage

III. Etiology

Automobile accidents

Sports

Falls


2 stages in post-traumatic period :

Early stage of spinal shock and increasing impairment

Initial period of spinal shock :

All neurologic activity ceases @ , below, and slightly above the level ofinjury

No reflexes are present May persist days or weeks

During period of spinal shock :

Flaccid paralysis Sensory loss @ and below the injured area

Absence of all reflex responses Loss of central control of autonomic function

In pt with cervical injury :

o Loss of control of vasomotor tone

o

BP is low and labile

o Diaphoresis

o Loss of control in body temp and bowel and bladder emptying

o

Urinary retention and paralytic ileus

Recovery and recognition of extent of functional loss

Gradual return of reflex activity below the level of injury

No impulses including reflexes can pass through specific area of

damaged neurons

Hyperreflexia develops due to normal inhibitory or “dampening”

impulses that cannot reach the cord levels below the injury

Spastic paralysis

Sensory deficits

Reflex / neurogenic bladder and bowel function (urinary incontinence

and reflex defecation) are present below level of damage

--Specific effects of permanent damage depend on the level @ w/c the spinal

cord trauma occurred

Quadriplegia



o Paralysis of all 4 extremities

o

C1-C8

Paraplegia

o Paralysis of lower part of the trunk and legso

T1-L4

Partial cord injuries

o Can lead to diff patterns of impairment depending on point ofdecussation and loc. of specific injured tracts :

- ipsilateral paralysis

- contralateral loss of pain and temp sensation

Autonomic dysreflexia

o

With injury of cervical spine, stimulation of the sympatheticsystem may result in this

o A potentially serious complicationo

Caused by a sensory stimulus that triggers a massive

sympathetic reflex response that cannot be controlled from

the brain

o Trigger may be any noxious stimulus in the body but most

frequently is a distended bladder or decubitus ulcer

o

A sensory stimulus to SNS below level of injury can stimulate

entire chain of SNS ganglia , leading to :- excessive vasoconstriction

- sudden increase in BP

- severe headache- visual impairment

o Bradycardia accompanies this syndrome :

- as the Baroreceptors sense the high BP and respond through

the vagus nerve by slowing the HRo Excessive vasoconstriction cannot be reduced through the

cardiovascular control center

o Finding and removing the cause of stimulus and Administering

meds to lower BP to prevent stroke or heart failure

Complications are common after spinal cord injury due to :

o Immobility

o

Loss of function

o Muscle spasms – contractures

o Decubitus ulcers

o Resp and urinary infections Sensory and psychological components of sexual response are usually

blocked by injury

o Men may have neurogenic reflex erections

o Many men , particularly those with high-level cord injuries areinfertile because sperm production in testes is impaired

V. Treatment

Traction / Surgery – to relieve pressure and repair tissue

Glucocorticoids (methylprednisolone) – to reduce edema and stabilize

vascular system Ongoing care to prevent complications r/t immobility

Acute Neurologic Disorders2

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