Pathophys ch22 Acute Neuro Disorders Flashcards
Skull
- rigid bone connected by sutures
Meninges
- three continuous CT membranes covering the brain and spinal cord
Cerebrospinal fluid (CSF)
- clear liquid that provides a cushion for the brain and spinal cord
Blood-brain barrier and blood-CSF barrier
- impermeable capillaries in the brain limit the passage of potentially damaging materials into the brain and controls the delicate balance of electrolytes, glucose, and proteins in the brain and CSF
Prefrontal area
- Functional area
- Frontal lobe
- intellectual function and personality (thinking)
Premotor cortex
- Functional area
- Frontal lobe
- skilled movements (back of frontal lobe)
Motor cortex
- Functional area
- Frontal lobe
- voluntary movements
Broca’s area
- speech (expression, formation of words)
- located on the left side usually
Parietal lobe
- sensation (touch, pain etc.)
Occipital lobe
- vision (back of head)
Auditory cortex
- Temporal lobe - hearing
Olfactory cortex
- Temporal lobe - smell
Wernicke’s area
- Temporal lobe - comprehension of speech or memory
Cerebellum
- balance, position, coordinated movement
Medulla oblongata
- control and coordinating centers for life sustaining functions (ie. breathing and HR)
Hypothalamus
- maintains homeostasis
Thalamus
- sensory sorting and relay center
Basal nuclei
- coordination and control of body movement
Reticular activating system
- arousal and awareness
Limbic system
- emotional response
Spinal Cord
- the cord consists of nerve fibers or tracts or surrounding nerve cell bodies
Anterior horns
- spinal cord - cell bodies of motor neurons whose axons leave the spinal cord (efferents) to innervate skeletal muscle
Posterior horns
- spinal cord - association (interneurons) neurons
Ascending fibers
- spinal cord - sensory nerve fibers (afferents)
Descending fibers
- spinal cord - motor nerve fibers
Reflexes
- automatic or rapid or involuntary response to a stimulus.
Reflex pathway
- Sensory stimulus receptor ==> afferent nerve fiber ==> synapse in spinal cord ==> efferent never fiber ==> response at effecter site
Reflex pathophysiology
- absent, weak or abnormal responses may indicate the presence of a neurologic problem in the brain or spinal cord
Neurons
- are specialized nonmitotic cells that conduct impulses throughout the CNS and PNS - (cell bodies do not mitose)
Neuron architecture
- Consists of cell body, dendrites and axons
Glial cells
- support and protect the neurons
Local (focal) effects
signs related to the specific area of the brain or spinal cord in which the lesion is located
Left hemisphere damage
loss of logical thinking ability or analytical skills or other intellectual abilities and communication skills
Right hemisphere damage
impairs appreciation of music and art and causes behavioral problems or spatial orientation (what is going on around you)
Consciousness centers
The cerebral cortex and the RAS in the brainstem determine the level of consciousness
Consciousness – supratentorial lesions
Extensive supratentorial lesions must be present in the cerebral hemispheres to cause loss of consciousness
Consciousness – infratentorial lesions
Small lesions in the brainstem can affect the RAS (reticular activation system)
Consciousness – blood pathophysiology
Acidosis or hypoglycemia can depress the CNS reducing the level of consciousness (ie diabetes)
Coma
Person does not respond to painful or verbal stimuli and the body is motionless with some reflexes present (can come out of it)
Vegetative state
loss of awareness and mental capabilities resulting from diffuse brain damage although the brainstem continues to function (can not come out of it)
Lock-in syndrome
person is aware and capable of thinking but is paralyzed and cannot communicate
Brain death criteria
Cessation of brain function, absence of brainstem reflexes, absence of spontaneous respiration, (medulla oblongata function absent), independent establishment of certainty of irreversible brain damage by two Dr at two times.
Motor dysfunction – upper motor neurons
Damage to UPPER MOTOR NEURONS in the frontal lobe or to the corticospinal tracts in the brain causes weakness or paralysis on the opposite side of the body, muscle tone and reflexes may be increased
Motor dysfunction – lower motor neurons
Damage to lower motor neurons causes weakness or paralysis on same side of the body, muscles are flaccid (limp) and reflexes are absent
Sensory dysfunction
loss of touch, pain, temperature, position or special senses
Visual loss (hemianopia)
- loss of visual field depends on the site of damage in the visual pathway
Expressive aphasia
Language disorders - cannot speak or write fluently; motor problem
Receptive aphasia
(Language disorders) unable to understand written or spoken word
Global aphasia
(Language disorders) cannot express self or comprehend other’s language; both speaking and understanding
Fluent aphasia
(Language disorders) pace of speech is normal but contains made-up words and sentences that do not make sense, ie. stroke
Nonfluent aphasia
(Language disorders) slow and labored speech with short phrases
Dysarthria
(Language disorders) words cannot be articulated clearly (difficult speech due to cranial nerve damage)
Agraphia
(Language disorders) impaired writing ability
Alexia
(Language disorders) impaired reading ability
Agnosia
(Language disorders) loss of recognition or association (a=without or gnosia=knowledge)
Seizures
- spontaneous excessive discharge in the brain (over working of the brain)
Increased intracranial pressure (ICP)
Results in decreased blood flow to the area compressed causes tissue necrosis. ICP due to inflammation, blood leakage, tumor, etc. in the brain. Common in many neurologic problems
Increased intracranial pressure (ICP) - Early signs
severe headache, vomiting, papilledema
Increased intracranial pressure (ICP) - Vital signs
increasing BP, slowed HR, reduced respiratory rate
Herniation
brain tissue is displaced by blood clot or tumor (pushed out of place)
Brain tumors
Tumors, both benign and malignant, are space-occupying lesions that cause increased ICP and localized dysfunction related to their location
Primary malignant brain tumors
do not have well-defined margins but are invasive and have irregular projections into adjacent tissue
Secondary brain tumors
metastasize from breast or lung tumors
Brain tumors - Signs and Symptoms
Increased ICP, morning headache, vomiting, seizures
Vascular disorders affecting the CNS
hemorrhagic or ischemic in origin
Vascular disorders – pathophysiology
Interference with blood supply to a specific area of the brain results in local damage and manifestations depending on the particular cerebral artery involved
Transient ischemic attacks (TIAs)
Temporary localized reduction of blood flow in the brain
Recovery within 24 hours
Transient ischemic attacks (TIAs) – Etiology
atherosclerosis, embolus, vascular spasm, or local loss of autoregulation
Transient ischemic attacks (TIAs) – S&S
Intermittent short episodes of impaired function
Cerebrovascular accident (stroke)
infarction of brain tissue that results from lack of blood (ischemia)
Cerebrovascular accident (stroke) – Seriousness
five minutes or less of ischemia causes irreversible cell damage
Cerebrovascular accident (stroke) – Pathophysiology
A central area of necrosis develops surrounded by an area of inflammation. Function in this area is lost immediately. The tissue liquefies leaving a cavity in the brain
Cerebrovascular accident (stroke) – Etiology, 3 types
- occlusion by atheroma
- obstruction by an embolus
- an intracerebral hemorrhage by a ruptured artery
Cerebrovascular accident (stroke) – S&S
weakness, numbness, loss of vision or speech, severe headache, dizziness or unsteadiness
Cerebral aneurysms
localized dilation of an artery – often at the points of bifurcation on the circle of Willis
Cerebral aneurysms – Pathophysiology
Enlarge over the years until compression of nearby structures causes clinical signs or rupture. Rupture often results from a sudden increase in blood pressure during exertion
Cerebral aneurysms – affect of blood
blood causes inflammatory response and irritation of nerve roots
Cerebral aneurysms – S&S
visual disturbances, headache, photophobia, periods of dysfunction or nuchal rigidity
Meningitis
infection of the meninges of the CNS
Meningitis – pathophysiology
Inflammatory response to the infection leads to increased ICP. Purulent exudates covers the surface of the brain and is present in the CSF. Blood vessels on the surface of the brain appear dilated.
Meningitis – S&S
severe headache or back pain or photophobia or nuchal rigidity
Brain abscess
localized infection, frequently in the frontal or temporal lobes
Brain abscess – pathophysiology
Necrosis of the brain tissue and an area of edema
Brain abscess – etiology
It usually results from ear, throat, lung, or sinus infection
Encephalitis
viral infection of the CT in the brain and spinal cord
Encephalitis – pathophysiology
Necrosis and inflammation develop in the brain tissue
Encephalitis – S&S
severe headache, stiff neck, lethargy, vomiting, seizures, fever
Rabies
Viral infection from the bite of a rabid animal
Rabies – pathophysiology
It causes severe inflammation and necrosis of the brainstem and basal ganglia
Rabies – S&S
headache, fever or neuron hyperirritability
Tetanus
SPORE-FORMING Bacterial infection – spores can survive for years in soil
Tetanus – pathophysiology
Produce an exotoxin that enters the nervous system and causes tonic muscle spasms
Tetanus – S&S
S&S - jaw stiffness, difficulty swallowing, stiff neck, muscle spasm
Poliomyelitis
VIRAL infection that attacks motor neurons of the spinal cord and medulla and results in minor flulike effects to paralysis
Herpes zoster (shingles)
A VIRAL infection in adults seen years after chickenpox
Herpes zoster (shingles) – pathophysiology
Usually affects one cranial nerve or one dermatome on one side of the body
Herpes zoster (shingles) – S&S
pain, paresthesia and vesicular rash
Postpolio syndrome
occurs 10-40 years after recovering from polio with progressive and debilitating fatigue, weakness, pain, and muscle atrophy
Reye’s syndrome
linked to viral infections in young children that have been treated with aspirin
Reye’s syndrome – pathophysiology
Noninflammatory cerebral edema develops and an enlarged liver
Reye’s syndrome – S&S
lethargy, headache, vomiting, disorientation, hyper-reflexia
Guillain-Barre syndrome
inflammatory condition of the peripheral NS
Guillain-Barre syndrome – Etiology
Abnormal immune response precipitated by a viral infection or immunization
Guillain-Barre syndrome – pathophysiology
Local inflammation, accumulated lymphocytes, demyelination, and axon destruction.
Guillain-Barre syndrome – Course of disease
Inflammation begins in the legs and ascends to the trunk and neck or ascends to involve the diaphragm and respiratory muscles. Reversible if treated early.
Guillain-Barre syndrome – S&S
progressive muscle weakness and areflexia beginning in legs
Concussion
reversible interference with brain function from sudden excessive movement of the brain disrupting neurologic function and leading to loss of consciousness
Contusion
bruising of brain tissue with rupture of small blood vessels and edema
Closed head injury
skull is not fractured but brain tissue is injured and blood vessels may be ruptured
Open head injury
fracture of the skull or penetration of the brain by missiles or sharp objects
Contrecoup injury
area of the brain contralateral to the site of direct damage is injured as the brain bounces off the skull
Primary brain injury
direct injury such as laceration or crushing of the neurons, glial cells and/or blood vessels of the brain
Secondary brain injury
result from effects of cerebral edema, hemorrhage, hematoma, cerebral vasospasm or infection and ischemia
Head injuries
Any trauma to the brain causes loss of function in the part of the body controlled by that area of the brain
Head injuries – pathophysiology
Cell damage and bleeding lead to inflammation or necrosis and tissue replaced by scar tissue or a cyst
What is a hematoma?
Collection of blood in the tissue that develops from rupture of blood vessels. ie. bruise
Epidural hematoma
bleeding between the dura and skull
Subdural hematoma
bleeding between the dura and arachnoid
Subarachnoid hemorrhage
bleeding between the arachnoid and pia
Intracerebral hematoma
bleeding inside the cerebrum
Effect of hematomas.
Bleeding leads to local pressure on the tissue and increased ICP
Head injuries - S&S
seizure, cranial nerve impairment, otorrhea, rhinorrea, or otorrhagia
Cervical spine injuries - hyperextension or hyperflexion
hyperextension or hyperflexion of the neck with possible fracture along with damage to the disc and ligaments leading to dislocation or loss of alignment of vertebrae and compression or stretching of the spinal cord
Cervical spine injuries – Dislocation
Dislocation of vertebrae may crush or compress the spinal cord and compromise blood supply
Compression fracture (Spinal cord injuries)
great force is applied to the top of the skull or to the feet and is transmitted down or up the spine, shattered bone is compressed and protrudes, exerting pressure against the cords
Penetration injuries (Spinal cord injuries)
stab or bullet wound
axon
Neuron cell bodies in the spinal cord do not regenerate but __________ regrowth may occur
transection or crushing
Complete __________ of the cord causes irreversible loss of sensory and motor function at and below the level of injury
Effect of prolonged ischemia and necrosis
permanent cell and tissue damage
Spinal cord injuries - (S&S) During spinal shock
- Flaccid paralysis or sensory loss at or below the injury
- Absence of all reflex responses and loss of central control of autonomic function
Spinal cord injuries - (S&S) Recovery
Gradual return of reflex activity below the injury
Hyper-reflexia develops
Cervical spine injury may result in autonomic dysreflexia
sensory stimulus triggers a massive sympathetic reflex response that can’t be controlled by the brain
