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 ns
o 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 this
o If pressure inside the skull increases in infants before sutures
fuse or ossify , cranial bones may separate causing the head to
enlarge
Foramina :
o Cavities /Openings in skull
o Canals through which nerves and blood vessels pass
o Largest opening is the Foramen magnum , located in the
occipital bone @ the base of the skull where the spinal cord
emerges
Meninges
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 villi
o Projections of arachnoid into the dural sinuses @ several
places around brain through w/c CSF can be absorbed into
the venous blood
Pia mater
o Inner layer
o Delicate connective tissue
o Adheres closely to all convolutions on the surface of the brain
o Many small blood vessels can be found
CSF
Characteristics :
o Appearance clear and colorless
o Pressure 9 to 14 mm Hg or 150 mm H20
o RBC - None
o WBC Occasional
o Protein 15 to 45 mg/dL
o Glucose 45-75 mg/dL
o 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 mL
o 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 (eg.
osmoreceptors in hypothalamus)
Blood-brain barrier
@ choroid plexus
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 the
spinal cord
- occur as association fibers, connecting diff gray areas in
the brain
Each hemisphere
o Divided into 4 major lobes , each of w/c has some specific
functions
o Concerned with voluntary movements and sensory function in
the opposite (contralateral) side of the body
Frontal Lobe
o Prefrontal area intellectual function and personality
o Premotor cortex skilled movements
o Motor cortex voluntary movements
o Brocas area speech (expression)
Parietal Lobe
Diencephalon
Medulla oblongata
Contains the :
o Vital control centers that regulate respiratory and
cardiovascular function
o Coordinating centers that govern cough reflex, swallowing and
vomiting
Located dorsal to the pons and medulla , below the occipital bone
V. Cranial 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
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 motor
neurons 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 fibers
from 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
Phrenic nerve
- consists of fibers from spinal nerves C3-C5
Sciatic nerve
- contains fibers from spinal nerves L4-L5 and S1-S3
The dispersal pattern can minimize the effects on a muscles
contraction of damage to one spinal cord segment
III. Reflexes
I. Neurons
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
Neurotransmitter is released
from vesicles
Neurotransmitter flows
across the synaptic cleft
Neurotransmitter act on
receptor in postsynaptic
membrane
Stimulus / Response
Inactivated by enzymes
II. Parasympathetic NS
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 the
spinal cord
Ganglia
o 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
actions
o Cholinergic fibers / Acetylcholine
- the neurotransmitter released by preganglionic fibers at the
ganglion
- 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 receptors
o 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 effect
o 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
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 digestive
tract
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 the
organ
Cholinergic blocking agents
o Reduce PNS activity
Cholinergic / Anticholinesterase agents
o Prevent the enzyme cholinesterase from breaking down Ach
o Increases PNS activity
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 L
frontal lobe
o Loss of vision that results from damage to the occipital lobe
o With an expanding lesion (eg. growing tumor/ hemorrhage) ,
addtl impairment is noted as the adjacent areas become
involved
Motor dysfunction
L and R hemispheres
LOC
-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 cerebral
hemispheres
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 Temp
o Position
o Special senses of vision, hearing , taste and smell
Somatosensory cortex in parietal lobe
Seizures
Language Disorders
Aphasia
o Inability to comprehend or to express language
o 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 or
construct a meaningful senstence
o Occurs when Brocas 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 is
meaningless
o Damage to Wernickes area in L temporal lobe
Global aphasia
o Combination of expressive and receptive aphasia
o Results from major damage to the brain including Brocas
area, Wernickes area and many communicating fibers
throughout brain
Other types
Dysarthria
o Words cannot be articulated clearly
o 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
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
Visual Signs
Papilledema
Pressure on oculomotor nerve (cranial nerve III) affects size and
response of pupils
o One pupil ipsilateral to the lesion becomes fixed
(unresponsive to light) and dilated as PNS fibers in affected
oculomotor nerve become nonfunctional
o With an addtl pressure increase, both pupils become fixed
and dilated
Ptosis / droopy eyelid
o Another effect of pressure on cranial nerve III
o Innervation to the muscle of upper eyelid is impaired
Nystagmus
o Abnormal or excessive eye movements
Changes in CSF
A specimen may be procured with a lumbar puncture by inserting a
fine needle bet vertebrae @ L3-4 , into SA space and withdrawing a
small sample of CSF
A manometer may be attached to the syringe to measure pressure
Pressure of CSF is elevated in pt with increased ICP (above 20 mm
Hg)
Composition of CSF may vary with the cause of problem ;
o Pinkish in color and contain erythrocytes = hemorrhage
o Cloudy, yellowish fluid and contains numeours WBCs =
infection
o Abnormal CHON levels in CSF = neoplasm
Herniation
Diagnostic Tests
CT scans
MRI
Cerebral angiography
Doppler utz (assess patency of carotid and intracerebral vessels)
EEG
Radionuclide/ technetium (tract movement in CNS)
Lumbar puncture (check pressure and analyze CSF for altered
components)
Glasgow coma scale (assess LOC)
Checklist of normal reflexes
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 tumors
o 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 MRI
o Stereotactic biopsy
II. Pathophysiology
III. Etiology
V. Treatment
May be caused by :
o Partial occlusion of an artery caused by atherosclerosis
o 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
Ruptured
cerebral vessel
Lack of blood in
brain tissue
Tissue
necrosis/Infarction
Tissue liquefies
Cavity in brain
I. Pathophysiology
II. Etiology
Risk factors :
o DM
o HTN
o Systemic lupus erythematosus
o 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 been
well 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
Depend on :
o Location of obstruction
o 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 until
several 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 signs
o 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 artery
o Supplies the occipital lobe
o Visual loss is likely if it is occluded
o
o
o
o
o
o
o
o
IV. Treatment
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
After rupture :
Surgical clipping may also be done
There is substantial risk of rebleeding @ the site of repair or from
other aneurysms
Addtl therapeutic measures focus on reducing effects of :
Increased ICP
Cerebral vasospasm
Infections (5)
Meningitis
I. Definition
II. Pathophysiology
III. Etiology
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 treatment
o 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 young
children
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)
IV. Signs and Symptoms
VI. Treatment
VII. Prognosis
Brain Abscess
Encephalitis
Lastly ..
o
Pain and Swelling may develop in large joints
o Sometimes progressing to chronic arthritis
Prolonged therapy w/ antimicrobials such as doxycycline is prescribed
Rabies (hydrophobia)
Tetanus (lockjaw)
Polio virus
o Highly contagious through direct contact or oral doplet
o Reproduces in lymphoid tissue in oropharynx and digestive
tract , then enters blood and eventually CNS
o Attacks the motor neurons of the spinal cord and medulla ,
causing minor flulike effects in many cases, but paralysis and
resp. failure in other cases , depending on level of destruction
Sx :
o Fever
o Headache
o Vomiting
o Stiff neck
o Pain
o Flaccid paralysis
Infection-Related Syndromes
Reyes 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 failure
o Jaundice is not present, but serum levels of liver enzymes are
elevated
o 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 Headache
o Vomiting
w/c are quickly followed by :
o disorientation
o Hyperreflexia
o Hyperventilation
o Seizures
o Stupor
o 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 or
immunization may be responsible
Local inflammation accompanied by :
o Accumulated lymphocytes
o Demyelination
o Axon destruction
IV. Treatment
Head Injuries
III. Pathophysiology
I. Definition
May involve :
o Skull fractures
o Hemorrhage
o 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
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 delay
onset 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 the
brain and brainstem as the head swings
Objects that fall on head
Blow to he head
Seizures
o 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 Pneumonia
o Decubitus ulcers
VI. Treatment
II. Pathophysiology
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 addtl
compression , but as edema subsides , there may be partial recovery
of 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 diaphragm
o 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
V. Treatment