Chapter 16 - Disorders Of CNS, PNS, NMJ Flashcards
Alterations of CNS function
Involve traumatic injury, vascular disorders, tumour growth, infections and inflammatory processes
Alterations of PNS function
Involve nerve route, nerve plexus, nerves themselves or neuromuscular junction
Primary cause of death and disability in individuals under age of 40
traumatic brain injury
What is the percentage of TBIs sustained by children and youth and why?
30%
-usually sports and recreational activities
TBI
Alteration in brain function or other evidence of brain disease caused by an external force
Primary TBI
Direct impact
-focal or diffuse
what is focal and diffuse, and what are the percentages of
Focal- affecting one area 2/3
Diffuse- involving more than one, atonal injury 1/3
Secondary TBI
Indirect result of primary injury
-systemic responses and cascade of cellular/molecular cerebral events
TBI diagnosis
Glasgow coma scale (GCS)
Score 2
Eye opening to pain, incomprehensible sounds, extension to pain
Score 3
Eye opening to verbal command, inappropriate words, flexion to pain
The lower the score the
More severe the damage
Primary focal
Can be closed or open injury
Closed primary focal
More common
-head striking hard surface, moving object striking head or blast waves
-dura mater remains intact, brain tissue not exposed
Open primary focal
Penetrating trauma or skull fracture
-break in dura mater, brain tissue is exposed
Severe cases of primary focal closed brain injury
Contusions, epidural, subdural, hematomas
Mild primary focal closed BI
80 percent of cases
Coup or contrecoup
Coup= injury at site of impact
Countrecoup= injury from brain bouncing back and hitting opposite side of skull
Contusions
Compression of skull at point of impact produces a contusion
-blood leaking from injured vessel
Smaller contact area =
More severe the injury
Edema forms which increases ICP =
Hemorrhages, edema, infarction, necrosis and tissue becomes pulpy
Most common site of contusions
Frontal lobe
Greatest injury effects how many hours after injury
18-36 hours
Diagnosis for contusions
Glasgow coma scale, CT scan or MRI
TX for contusions
Surgical removal of large contusions and areas of hemorrhage may be required
Epidural
Skull fracture, hemiparesis, pupil dilation, loss of consciousness
Subdural
Fast/hemianopia or alcohol, craniotomy, membrane forms around hematoma
Intracerebral
Frontal temporal, penetrating steering, pupil dilation, positive babinksi
Epidural hematomas
Bleeding between dura mater and skull
-artery bleeding, hematoma
Most common site of epidural hematomas
Temporal fossa
Most common site of epidural hematomas
Temporal dosas
Symptoms and epidural hematomas
-lose consciousness
-as it grows, more headache, confusion, seizure
-hemiparesis
-pupil dilation
Hemiparesis
Weakness or inability to move one side of body
Pupil dilation and prognosis
Injury prognosis is good if treated before both pupils dilate
TX for epidural hematomas
Medical emergency
Subdural hematomas
Bleeding between dura mater and brain
Acute subdural hematomas
Develop quickly, within hours
-as it grows, ICP rises and pressure is applied to veins assisting in short term limitation
Symptoms for acute subdural hematomas
Headache/confusion
-hemianopia
-anopia
Hemianopia
Blindness over half of vision field
Anopia
Blindness
Chronic subdural hematomas
Develop over weeks to months
-common in alcohol abuse
-mass bleeding, subdural space fills with blood
-formation of vascular membrane around hematoma
Symptoms of chronic subdural hematomas
Headaches, tenderness over hematoma
-worsening dementia, paratonia (rigidity)
TX for chronic subdural hematomas
Craniotomy to remove jelly like blood
Intracerebral hematomas
Bleeding within the brain
-2 to 3 percent of head injuries
-frontal and temporal lobe
Intracerebral hematomas: penetrating and shearing forces injure small blood vessels =
Growing mass/edema
Symptoms of Intracerebral hematomas
Sudden rapid decrease in level of consciousness
-pupil dilation, positive babinski reflex
Positive babinski reflex
When big toe bends up and back of food and other toes fan out
Examples of primary focal closed
-coup/contrecoup
-contusion
-epidural hematoma
-subdural hematoma
-Intracerebral hematoma
Primary focal open
Compound skull fracture/ missile injuries
Primary diffuse injury
Diffuse brain injury
Open brain injury
Trauma penetrates dura mater and creates both focal and diffuse injury
-compound skull fractures and misleading injuries
Compound skull fracture
Opens a path between cranial contents and environment
-whenever cuts of the scalp, tympanic membrane, sinuses, eye or mucous membranes occur a CSF should be considered
Cause of CSF are crush or stretch injury
Crush: includes cutting or crushing - whatever missile touches
Stretch: blood vessels and nerve damage - without direct contact
Most open brain injury become
Unconscious
Basilian skull fractures
Usually caused by substantial blunt force trauma
-at least one of the bones that compose base of skull
-generate spinal fluid leaking from ear to nose = blackened eyes
Diffuse brain injury =
Injury widespread in brain
Primary diffuse brain injury
Effects from high levels of acceleration and deceleration or rotational forces
-can shear axonal fibres + white matter tracts
Degree of shearing =
Cognitive consequences = extensive cognitive impairments
Degree of shearing =
Cognitive consequences
Diagnosis of primary diffuse injury
Electron microscope to detect axonal damage
Secondary brain injury
Indirect result of primary brain injury, including both trauma and stroke syndromes
Systemic
Hypotension, hypoxia
cerebral
Inflammation, edema, inc ICP
Primary effects cause
Disruption to BBB causing neuronal death
Management of secondary brain injury
-prevent hypoxia, maintain cerebral perfusion pressure and removal of hematomas
-nutritional management is critical
mild TBI
Mild concussion
-immediate transitory clinical manifestations
Mild TBI consciousness
Less than 30 min
Glasgow score for mild TBI
13-15
Symptoms of mild TBI
Headache, nausea, vomiting
Diagnosis of mild TBI
Blood test to determine need for CT scan
Moderate TBI
Moderate concussion
-permanent defects in arousal and attention
Moderate TBI consciousness
Lasts more than 30 mins up to 6 hours
Glasgow score for a moderate TBI
9-12
Symptoms of moderate TBI
Confusion, amnesia (more than 24 hours), brain imaging is abnormal
Severe TBI
Severe concussion
-permanent damage to vegetative state to death
Consciousness and Glasgow score for a severe TBI
More than six hours, 3-8
Signs of severe TBI
-Change in Pupillary reaction, cardiac and respiratory systems
-decorticate or decerebrate posturing
-inc ICP 4-6 days after injury
Symptoms of a severe TBI
Compromised coordinated movements, verbal and written communication
TX fro severe TBI
Maintain cerebral perfusion and promote neural protection
Complications of TBI
Severity and brain location determine probable complications
Post concussion syndrome
Lasts weeks to months after concussion
-important to have 24 hours of close observation
Post concusssion syndrome symptoms
-drowsiness, confusion, vomiting
-unequal pupils
-csf drainage from ears or nose
-double vision
Post traumatic seizures
Epilepsy
-10 to 20 percent of TBI
Molecular changes = sprouting of new hyperexcitable neural activity = inc seizures
Highest risk for post traumatic seizures
Open brain injuries
Chronic traumatic encephalopathy
Progressive deleting disease that develops with repeated brain injury
-contact sports, blast injuries
Chronic traumatic encephalopathy consequences
Violent behaviour, change in cognitive, motor function, depression, suicide
What tangles occur in brain (chronic traumatic encephalopathy
Tau neurofibrillary
Who are particularly at risk for spinal cord and vertebral injury
Males 20-39 yoa, adults 79+ yoa
Primary spinal cord injury
Injury occurs if an injured spine does not receive adequate immobilization following trauma
C1-C4 is
Life threatening due to loss of CV and respiratory function
Secondary spinal cord injury
Disease causing process occurring within minutes and continues for weeks
-hemorrhage in grey matter (death of entire grey matter)
Cord swelling =
Inc dysfunction = difficult to distinguish permanent and temporary damage
Death of oligodendrocytes =
Myelin degeneration
Vertebral fractures, dislocation, bone fragments =
Shearing and compression
Vertebrae fracture easily due to
Torn supporting ligaments
Vertebral injuries occur at the
Most moveable portions of column
Hyperextension
Disruption of intervertebral discs
Flexion
Vertebral wedge fracture
Rotation
Shearing force and rupture of ligament support
Manifestations of vertebral injuries: spinal shock
Immediate development, loss of function at or below level of injury
-hypothalamus cannot regulate body heat, person assumes temperature of air
Poikilothermic
Person assumes temperature of air
Spinal shock lasts, and returns
Lasts: 7-20 days
Returns: with reflex emptying of bladder
Manifestations of vertebral injuries: neurogenic shock
Occurs with injury above T6
-unopposed parasympathetic activity
-results in vasodilation and hypotension
Migraine
Episodic, genetic, environmental, hyperoccipital (vision)
Cluster headaches
Many attacks per day, remission, trigeminal nerve
Tension headaches
Episodic, tight band around head, trigeminal nerve
Three classifications of migraines
- With aura
- Without aura
- Chronic
Occurrence of migraines in Canada (men, women, children)
M- 8
W- 25
C-10
Aura
Beings as spreading neural hyperactivity in occipital brain region
-visual processing regions
Premonitory phase
Symptoms occur hours to days before onset of aura
-tired, irritable
Migraine aura
1/3 of persons have aura symptoms that last up to 1 hour
Headache phase
Begins on one side of head, spreads to entire head
Recovery phase
Irritability, fatigue
Who primarily has cluster headaches
Men 20 to 50 yoa
Pathophysiology of cluster headaches
Pain related to neurogenic inflammation
-sympathetic under activity and parasympathetic
TX for cluster headaches
Oxygen inhalation, sumatriptan
Age of onset for tension type headaches
10-20 yoa
Cause of tension type headaches
Hypersensitivity of pain fibres from trigeminal nerve
TX for tension type headaches
Mild TTH treated with ice, more severe with aspirin
Meningitis vs encephalitis
M- infection of meninges and subarachnoid space
E- inflammation within brain
Bacterial meningitis
-infants and children
-strep, s.pneumoniae, e.coli
Pathogens cross BBB into CSF then release toxins
-ICP occur due to black age of CSF
Progressive symptoms of bacterial meningitis
Spinal rigidity, seizures, positive babinski reflex
Viral meningitis
May be direct infection or secondary to disease such as measles, mumps, herpes
Viral encephalitis
Virus can directly invade brain and cause inflammation, post infection may occur due to autoimmune response
Multiple sclerosis
CNS demyelination, T and B cells cross BBB attack myelin, activation of micro Gaia
Multiple sclerosis
CNS demyelination, T and B cells cross BBB attack myelin, activation of micro Gaia
Guillain barr
PNS demyelination, secondary to other infections, recovery possible
Demyelination disorders
Result of damage to myelin nerve sheath and affect on neural transmission
Risk factors for multiple sclerosis
Epstein Barr virus, genetics
Patho of MS
T and B cells cross BBB and attack myelin
-activation of microglia cells
Resulting in death of neurons, brain atrophy, primarily white tissue
When does grey matter degeneration occur in MS
During later stages
Initial symptoms of MS
-Paresthesia (burning or prickling sensations)
diagnosis for MS
No single test to diagnose MS
TX for MS
Corticosteroids, immunosuppressants, plasma exchange
Patho for guilain barre syndrome
Demyelination of PN, secondary occurrence to respiratory or gastrointestinal infection
Recovery for Giulian barre syndrome
Weeks to years, 30 percent have residualk weakness
Symptoms of Giulian barre syndrome
Vary from tingling and weakness to leg paralysis and quadriplegia
TX for Giulian barre syndrome
Intravenous immunoglobulin used during acute phase
Most common NMJ disorder
Myasthenia Travis
Myasthenia Travis
Chronic autoimmune disease
-antibodies against ACh receptors on postsynaptic membrane
Thymoma
Tumour of thymus, associated with Myasthenia Travis
Pathophysiology for Myasthenia Gravis
AChR are not recognized as self, thymoma forms a T cell dependant IgG autoantibodies which block binding site of AChR to acetylcholine
-destroy receptor site
Manifestations of Myasthenia Gravis
Muscles of head area affected, dysphasia, diaphragm and chest wall muscles weaken
Diagnosis of Myasthenia Gravis
Detection of anti-AChR antibodies
TX for Myasthenia Gravis
Immunosuppressants, thymectomy for people with thymoma
Primary tumours
Arise from brain substance
-do not metastasize readily bc there’s no lymph channels in brain substance
Metastatic secondary tumours arise in
Organ systems outside brain and spread to brain
Metastatic secondary tumours arise in
Organ systems outside brain and spread to brain
Metastatic secondary tumours local effects:
compression causing decreased cerebral blood flow and inc ICP
Symptoms of Metastatic secondary tumours
Seizures, visual disturbances
What is more common primary or metastatic?
Metastatic tumours are 10 times more common Thant primary
Primary Intracerebral tumours are called
Gliomas
Risk factor for primary brain tumours
Ionizing radiation
-detaches electrons from other atoms as they pass thru matter
How are primary brain tumours graded
From I to IV (IV being the most lethal)
What is the most common glioma
Astrocytoma (75%)
astrocytoma
Grade III and IV
-survival less than 5 years
Oligodendroglioma
Slow growing, grade II
-primarily in white matter
-seizure is the first symptom
Meningioma
Begins in dura mater, located on wings of sphenoid bone
-seizure is first symptom
Ependymoma
More common in children, arise from ependymal cells with 70% change of tumours beginning in fourth ventricle
Lower back pain affects the area between
Lower rib cage and gluteal muscles with pain often radiating into lower legs
Acute LBP associated with
Muscle or ligament strain
Chronic LBP
Includes degenerative disc disease, spondyloysis and spondylolisthesis
Degenerative disc disease
Normal process of aging, genetic
Spondylolysis
Occurs in the pars interarticularis of vertebral arch
-degeneration or fracture of PI
-wear on the cartilage/bones of the neck
Spondylolisthesis
Froward slippage of a vertebra
Spinal stenosis
Narrowing of spinal canal
-causing pressure on spinal nerves or cord
Herniation of an intervertebral disk
Displacement of nucleus pulposus beyond intervertebral disc space
Nucleus pulposus
Herniation = compresses spinal nerve = local/radiated pain
Most affected discs
L4-L5, L5-S1
