CNS Flashcards
(205 cards)
1
Q
What is a traumatic brain injury?
A
A traumatic insult to the brain possibly producing physical, intellectual, emotional, social, and vocational changes
2
Q
What organizations use theGlasgow Coma scale
A
used to describe injury severity by the international and United States National Traumatic Coma Data Banks
3
Q
TBI classifications: Mild
A
GCS 13-15 - associated with a mild concussion
4
Q
TBI classification: Moderate
A
GCS 9-12 - associated with structural injury such as hemorrhage or contusion
5
Q
TBI classification: Severe
A
GCS 3-8 - associated with cognitive and/or physical disability or death
**loss of consciousness for 6hours or more
6
Q
What populations are at risk for TBI?
A
Infants 6 months to 2 years School-age children Adolescents and young adults 15-35 years of age People more than 70 years of age Men 1.5 times as likely to sustain a TBI Persons living in high-crime areas
7
Q
Blunt Trauma
A
- closed, nonmissile
- Head strikes hard surface or a rapidly moving object strikes the head
- The dura remains intact; brain tissues not exposed to the environment
- Causes focal (local) or diffuse (general) brain injuries
8
Q
Open Trauma
A
- penetrating, missile)
- Injury breaks the dura and exposes the cranial contents to the environment
- Causes primarily focal injuries
9
Q
What are the most common type of brain injury?
A
mild concussion and classic cerebral concussion
10
Q
Focal brain injury
A
- accounts for more than 2/3 of head injuries
- specific and involves observable brain lesions
- contusions
- intracranial bleeding that displaces brain tissue
- cerebral edema
- coup-contrecoup
11
Q
Diffuse axonal injury (DAI)
A
accounts for less than 1/3 however accounts for the greatest number of severely disabled survivors
12
Q
What are some causes of brain trauma?
A
- Falls 28%
- Motor vehicle crashes 20%
- Moving objects or moving against stationary objects 19%
- Assault 11%
- Sports-related events
- Blasts (military active duty personnel)
13
Q
Compound fractures
A
caused by objects striking the head with great force or by the head striking an object forcefully
14
Q
Basilar skull fracture
A
- occipital blow- fracture of occipital bone and across the petrous pyramid
- the cervical vertebrae upwardly impacting the base of the skull can produce a posterior fossa basilar skull fracture
15
Q
Coup
A
- directly below the point of impact against object
- shearing of subdural veins
- trauma to base of brain
16
Q
Contrecoup
A
- on the pole opposite the site of impact (within the skull)
- shearing forces through brain
17
Q
Coup-Contrecoup
A
- injuries happen in one continuous motion
- coup - wall
- contrecoup - rebounds
18
Q
Where are contusions commonly found?
A
- frontal lobes, particularly at the poles along the inferior orbital surfaces
- temporal lobes, especially in the anterior poles and along the inferior surface
- frontotemporal junctions
19
Q
The ______ the area of the impact, the greater the severity of injury because the force is _____ into a _____ area.
A
smaller; concentrated; smaller
20
Q
Contusions result in what type of changes?
A
- attention
- memory
- executive attentional function (motivation, planning,)
- affect
- emotion
- behavior
21
Q
What is the difference between focal contusions and hemorrhagic contusions?
A
focal contusions are superficial, involving just the gyri whereas hemorrhagic contusions may coalesce into a large, confluent intracranial hematoma
22
Q
What are the clinical manifestations of a contusion?
A
- immediate loss of consciousness (no longer than 5 mins)
- loss of reflexes
- transient cessation of respiration
- brief period of bradycardia
- decreased blood pressure (30secs - a few mins)
- a momentary increase in CSF pressure
- ECG and EEG changes on impact
23
Q
What evaluations do you want to do on someone with a contusion?
A
- complete history and physical exam
- skull and spinal xray
- CT
- MRI
24
Q
How is treatment directed with a patient who has a contusions?
A
controlling ICP and managing symtoms
25
What can contusions cause?
Extradural (epidural) hemorrhage or hematoma
Subdural hematoma
Intracerebral hematoma
26
Extradural Hematoma
- 85% arterial bleeding
- 15% meningeal vein or dural sinus injury
- 90% have a skull fracture
- The temporal fossa is the most common site of extradural hematoma caused by injury to the middle meningeal artery or vein
27
What is the common cause of an extradural hematoma?
-MVAs
| occasionally minor falls and sporting accidents
28
Posterior extradural hematomas are caused by what?
a fracture across the transverse sinus from an occipital blow
29
What are some clinical manifestations with a classic temporal extradural hematomas?
- LOC followed by a lucid period that lasts for a few hours to a few days
- headache of increasing severity
- vomiting
- drowsiness
- confusion
- seizure
- hemiparesis
- ipsilateral pupillary dilation and contralateral hemiparesis
30
Subdural Hematoma
- 10% to 20% of persons with traumatic brain injury
- MVAs are the most common cause
- 50% of subdural hematomas associated with skull fractures
- Falls (older adults, substance abuse)
31
Acute Subdural hematoma
- Develops within 48 hours
- Often located at the top of the skull
- As ICP rises the bleeding veins are compressed and thus bleeding is self-limited
32
What are some clinical manifestations of an acute subdural hematoma?
-headache
-drowsiness
-restlessness
-agitation
-slowed cognition
-confusion
progressing to..
LOC
respiratory pattern changes
pupillary dilation
homonymous hemianpia
33
Chronic Subdural hematoma
Develops over weeks to months
Older adults
Alcohol abuse
80% complain of chronic headaches and have tenderness at site of injury
34
What is the difference in the treatment of an acute vs chronic hematoma?
acute- clot evac through burr hole
| chronic- craniotomy and then perc drain
35
Subdural hematoma forms after head trauma that severs the ______ _____ from dura to brain.
bridging veins
36
What are intracerebral hematomas associated with?
MVAs, falls and contusions
37
Where do intracerebral hematomas commonly occur?
frontal and temporal lobes but may also occur in the hemispheric deep white matter
38
The intracerebral hematoma acts as an _____ _____. Resulting in _______ ICP and compreesion of brain tissues with ____ ____.
expanding mass; increased; resultant edema
39
What are some clinical manifestations of an intracerebral hematoma?
- decreased level of consciousness
- coma or a confusional state
- contralateral hemiplagia
- temporal lobe herniation
40
What is the treatment for intracerebral hematoma?
- evacuation or
| - reducing ICP and allowing the hematoma to absorb slowly
41
What are the two types of open trauma head wounds?
compound fracture and missile injuries
42
What is a compound fracture?
open communication between the cranial contents and the environment
43
When should a compound fracture be investigated?
whenever there are lacerations of the scalp, tympanic membrane, a sinus, an eye, or mucus membranes.
44
What can be injured with a basilar skull fracture?
cranial nerves
45
What are the two mechanisms of injury with missile trauma?
crush and stretch injury
46
What is a crush injury?
the laceration and crushing of whatever tissue the missile touches,
47
What is the amount of crush related to?
degree of fragmentation, deformity, size and shape
48
What is a tangential injury?
injury to the coverings of the brain (scalp)
49
What is a stretch injury?
involves blood vessels and nerves that are damaged without direct contact due to the amount of tissue stretched secondary to shape deformation and striking velocity
50
What causes primary increase in ICP with a stretch injury?
air compressed in front of a bullet exerts an explosive effect on entry, producing extreme distant tissue damage and an immediate primary increase in ICP
51
What causes secondary increase in ICP with a stretch injury?
edema
52
What are some clinical manifestations with an open head injury?
-LOC
53
How is a diagnosis of a compound fracture made?
- physical exam
| - xrays
54
What is a diffuse axonal brain injury?
-results from a shaking effect
55
What is the primary mechanism of injury with a DAI?
rotational acceleration but can also be acceleration/deceleration and shaking, inertial effect
56
What does the severity of a DAI correspond with?
Severity corresponds to the amount of shearing force applied to the brain and brainstem (mild, moderate, severe)
57
What is axonal damage?
Shearing, tearing, or stretching of nerve fibers
58
What is the definition of a mild concussion
Temporary axonal disturbances causing attention and memory deficits but no loss of consciousness
59
Mild concussion: grade I
I—confusion, disorientation, and momentary amnesia
60
Mild concussion: grade II
II—momentary confusion and retrograde amnesia
61
Mild concussion: grade III
III—confusion with retrograde and anterograde amnesia
62
Classic cerebral concussion: grade IV
- Disconnection of cerebral systems from the brainstem and reticular activating system
- Physiologic and neurologic dysfunction without substantial anatomic disruption
- Loss of consciousness (<6 hours)
- Anterograde and retrograde amnesia
- Uncomplicated (no focal injury)
- Complicated (focal injury)
63
What is postconcussive syndrome?
Headache, cognitive impairments, psychologic and somatic complaints, cranial nerve signs and symptoms
64
How is postconcussive treated?
- Reassurance and symptomatic relief
- Close observation for 24 hours by a reliable individual so immediate intervention can be obtained if delayed effects become severe
65
DAI can further be categorized into..
mild DAI
moderate DAI
severe DAI
66
Mild DAI
- coma 6-24hours
- death uncommon, but cognitive, psychological and sensorimotor deficit
- 30% display decerebrate or decorticate posturing
67
Moderate DAI
- widespread physiologic impairment
- actual tearing of some axons in both hemispheres
- basal skull fracture, a focal injury, commonly associated
- last more than 24 hours
- recovery incomplete
- GCS 4-8 then 6-8 by 24hours
68
Severe DAI
- involves severe mechanical disruption of many axons in both cerebral hemispheres
- initial GCS of 3 - 78% mortality
- initial GCS of 3-8 - 36% mortality
- immediate autonomic dysfunction
- increased ICP
69
Treatment for TBI
- CT and MRI
| - seizure meds
70
Spinal cord trauma most commonly occurs from what vertebral fractures?
simple fracture, compressed fracture, and comminuted fracture
71
Where are the most common vertebral injuries?
-C1-C2 (cervical)
-C4-C7
-T1-L1 (thoracic-lumbar)
these are the most mobile parts of the vertebral column
72
How does a primary spinal cord injury occur?
occurs if an injured spine is not adequately immobilized
73
What are some examples of a primary spinal cord injury?
- cord concussion
- cord contusion
- cord compression
- laceration
- transection - complete and incomplete, preserved sensation only,motor nonfunctional,motor functional
- hemorrhage
- damage or obstruction of spinal blood supply
74
How does a secondary spinal cord injury occur?
begins within mins after injury, microscopic hemorrhages appear in central gray matter and pia arachnoid that increase in size within 2 hours - edema in the white matter occurs impairing microcirculation
75
Hyperextension injury of the spine
- fracture and dislocation of posterior elements such as spinous processes, transverse processes, laminae, pedicles, or posterior ligaments
- results from forces of acceleration-deceleration and the sudden reduction in the anteroposterior diameter of the spinal cord
76
Where is the location of injury from hyperextension?
cervical area
77
Hyperflexion injury if the spine
- fracture or dislocation of the vertebral bodies, disks, or ligaments
- causes subluxation of vertebrae
- results from sudden and excessive force that propels the neck forward or causes an exaggerated lateral movement of the neck to one side
78
Where is the location of injury from hyperflexion?
cervical area
79
Vertical compression (axonal loading)
- shattering fractures
- spinal cord is contused directly by retropulsion of bone or disk material into the spinal cord
- results from a force applied along an axis from top of the cranium through the vertebral body
80
Where is the location of injury from vertical compression?
T12-L2
81
Rotational forces
- ruptures support ligaments in addition to producing fractures
- adds shearing force to acceleration-acceleration forces
82
Where is the location of injury from rotational forces?
cervical areas
83
What is spinal shock?
- characterized by a complete loss of reflex function in all segments below the level of the lesion
- involves skeletal muscles, bladder, bowel, sexual function, and autonomic control
84
Why does spinal shock result in disturbed thermal control?
-sympathetic nervous system is damage; causes faulty control of sweating and radiation through capillary dilation
85
How long does spinal shock last?
7-20days or as long as 3months
86
What are some indications spinal shock is terminating?
- reappearance of reflex activity
- hyperreflexia
- spasticity
- reflex emptying bladder
87
What shock can be seen in additional to spinal shock with cervical or upper thoracic cord injury?
neurogenic shock
88
What is neurogenic shock?
results as a loss of sympathetic outflow, causing vasodilation, hypotension, bradycardia and hypothermia
89
Explain the chemical and metabolic changes in a spinal cord injury.
- Release of toxic excitatory amino acids, accumulation of endogenous opiates, lipid hydrolysis with production of active metabolites, and local free radical release
- Produce further ischemia, vascular damage, and necrosis of tissues
- Necrosis consumes 40% of cross-sectional cord within 4 hours of trauma and 70% within 24 hours
90
What is autonomic hyperreflexia
- a syndrome of a sudden and dangerous increase in blood pressure that may occur at anytime after spinal shock resolves
- life threatening and requires immediate treatment
91
What is autonomic hyperreflexia associated with?
a massive, uncompensated cardiovascular response to stimulation of the sympathetic nervous system.
92
Where do individuals, affected by autonomic hyperreflexia, usually have a lesion?
T6 or above
93
How is autonomic hyperreflexia characterized?
- paroxysmal hypertension (up to 300 systolic)
- a pounding headache
- blurred vision
- sweating above the level of the lesion with flushing of the skin
- nasal congestion
- piloerection
- bradycardia
- often associated with a distended bladder or rectum
94
What is the pathophysiology of hyperreflexia?
Involves stimulation of the sensory receptors below the level of the cord lesion (bladder or bowel distention); the intact autonomic nervous system reflexively responds with an arteriolar spasm that increases blood pressure; baroreceptors in the cerebral vessels, carotid sinus, and aorta sense the hypertension and stimulate the parasympathetic system; the heart rate decreases, but the visceral and peripheral vessels do not dilate because efferent impulses cannot pass through the cord.
95
How can autonomic hyperreflexia be relieved?
emptying the bladder or bowels - can be facilitated by drugs, such as phenoxybenzamine
96
What is cervical spondylolysis?
a DDD in the cervical spine predominately C5-C6 and C6-C7
97
What is a thrombotic stroke?
Arterial occlusions caused by thrombi formed in arteries supplying the brain or in intracranial vessels
98
Name a few risk factors for stroke.
1. Arterial hypertension
2. smoking doubles the risk
3. diabetes 2.5-3.5x the risk ischemic stroke
4. insulin resistance - independent for ischemic stroke
5. Polycythemia and thrombocynthemia - ischemic stroke
6. elevated lipoprotein-a: ischemic
7. impaired cardiac function - ischemic
8. hyperhomocysteinemia - ischemic
9. nonrheumatic afib - fivefold increase for ischemic
10. Chlamydia pneumoniae
99
What is and embolic stroke?
Fragments that break from a thrombus formed outside the brain
100
What are the most common cause of hemorrhagic stroke?
hypertension, ruptured aneurysms, arteriovenous malformations and fistula, amyloid angiopathy and cavernous angioma
101
Lacunar stroke
microinfarct smaller than 1cm in diameter and involves small perforating arteries, predominately in the basal ganglia, internal capsules, and pons
102
How does a cerebral infarct result?
when an area of the brain loses blood supply because of vascular occlusio
103
How are intracranial aneurysms formed?
arteriosclerosis, congenital abnormality, trauma, inflammation, or infection; cocaine use has been linked to aneurysms formations
104
Where are most aneurysms located?
bifurcations in or near the circle of Willis
105
Saccular aneurysms (berry)
- result of a combination of congenital abnormality in the media of the arterial wall and degenerative changes
- rare in childhood
106
Fusiform aneurysms (giant)
- greater than 25mm in diameter
| - occur as a result of diffuse arteriosclerotic changes
107
Where are fusiform aneurysms commonly found?
basilar arteries or terminal portions of the internal carotid arteries
108
Mycotic aneurysms
arteritis caused by bacterial emboli - uncommon
109
Traumatic (dissecting aneurysms
caused by a weakening of the arterial wall by a fracture line, by a penetrating missile, or after neurosurgical or imaging
110
Cavernous angiomas
- sinusoidal collections of blood vessels without interspersed normal brain tissue
- rarely hemorrhage
111
Capillary telangiectasis
- dilated capillaries with interspersed normal brain tissue found deep in the brain, particularly in the brainstem
- hemorrhage rare
112
Venous angioma
- considered a subset of developmental venous anomalies that occur secondary to arrested development
- result is primitive embryologic veins in a radial pattern feeding a central vein
- rarely hemorrhage
- most common vascular malformations found at autopsy
113
What is an arteriovenous malformation (AVM)?
- arteries feed directly into veins though a vascular tangle of malformed vessels
- occur more frequently in males
- occur anywhere in the brain
114
Cerebral infarcts can either be _____ or ______.
ischemic or hemorrhagic
115
Ischemic Infarct - white stroke
-cyotoxic ischemic events and interaction between blood elements and and blood vessels combine to produce a brain injury
116
Explain how ischemic infarcted areas loss autoregulation of blood flow.
Loss of glucose and oxygen delivery > depletion of high-energy phosphate compounds > depolarization > glutamate release and cannot be reuptaken > promotes excess excess entry of extracellular calcium > activation of degrading enzymes > lactic acid > associated focal vasodilation
117
Hemorrhagic infarct- red stroke
- bleeding occurs into the area as a result of blood flow
| - reperfusion injury - oxidative stres
118
WHere do most hemorrhagic infarcts occur?
cerebral cortex
119
What is the primiary cause of cerebral hemorrhage?
hypertension
120
What is the treatment for CVAs?
1. specialized stroke team
2. aspirin
3. thrombolysis within 3 hours
acutely decreasing bp, neuroprotective agents, and surgical evac not shown to improve outcomes
121
What is the PREVENTION treatment for CVAs?
1. Antiplatelet therapy
2. lowering bp
3. anticoags - but not of benefit with a pt in NSR
4. Carotid endarterectomy
5. lowering cholesterol
122
What is a subarachnoid hemorrhage (SAH) ?
blood escapes from a defective or injured vasculature into the subarachnoid space.
123
What are some risk factors for SAH?
- Family history 7x more likely
- heavy alcohol use
- smoking
- anticoags
- birth control
- saccular intracranial aneurysm
- intracranial AVM
- hypertension
- head injuries
124
Pathophysiology of SAH
blood pumps into subarachnoid > inflammatory reaction > blood coats nerve roots, clogs arachnoid granules, and clogs foramina (impairing CSF) > increased ICP > decrease CPP > granulation tissue is formed > scarring and impairment of CSF > secondary hydrocephalus often results
125
What are the clinical manifestations of a SAH?
-headache
-change in mental status
-N/V
-visual or speech disturbances
-kernig sign
brudzinki sign
126
Kernig Sign
straightening the knee with the hip and knee in a flexed position produces pain in the back and neck region
127
Brudzinski sign
passive flexion of the neck produces neck pain and increased rigidity
128
Grade I SAH
neurologic status intact; mild headache; slight nuchal rigidity
129
Grade II SAH
Neurologic deficit evidenced by cranial nerve involvement; moderate to severe headache with more pronounced meningeal signs
130
Grade III SAH
drowsiness and confusion with or without focal neurologic deficits; pronounced meningeal signs
131
Grade IV SAH
Stuporous with pronounced neurologic deficits; nuchal rigidity
132
Grade V SAH
deep coma state with decerebrate posturing and other brainstem dysfunction
133
Where so primary intracerebral tumors originate?
from brain substance, neuroglia, neurons, cells of the blood vessels, and connective tissue
134
What are the different types of primary intracerebral tumors?
- astrocytomas
- oligodendrogliomas
- mixed oligodendrogliomas
- ependymomas
135
What are astrocytomas?
- most common CNS tumors
| - develop from astrocytes and grow by expansion and infiltration into the normal surrounding brain tissue
136
How are grade I-IV of astrocytomas treated?
I - surgery and follow up CT
II - surgically or by conventional external radiation, local radiation, or stereostatic radiosurgery
III - surgery, radiotherapy, and chemotherapy
IV - surgery, radiotherapy, chemo, or placement wafers
137
What are olidoendrogliomas?
- far less common
- typically slow growing-growing well differentiated tumors, often with cyst and calcification present
- etiology unknown
138
What are ependymonas?
-gliomas that arise from ependymal cells that form the walls of the ventricles and grow either into the ventricle or into adjacent brain tissue, they are not encapsulated
139
Where are some common locations of ependymonas?
- 70% in the fourth ventricle; difficulty with balance, unsteady gait, uncoordinated muscle movement and difficulty with fine motor skills
- third ventricle
- lateral ventricles
- caudal portion of spinal cord
140
What are some clinical manifestations of ependymonas located in the third and lateral ventricles?
seizures, vision changes, contralateral weakness
141
What are the primary EXTRAcerebral tumors?
- Meningioma
- Nerve sheath tumors
- Metastatic carcinoma
142
What is a meningioma?
- sharply circumscribed mass that derives its shape from the space it occupies
- the cause is unknown
- arise from arachnoidal cap cells in dural coverings in brain
143
What are clinical manifestations of a meningioma based on?
```
based on site of origin:
sphenoidal wing
olfactory groove
parasagittal
parasellar
lateral convexity
```
144
What are some clinical manifestations of a meningioma originating from sphenoidal wing?
ophthalmoplegia, mild proptosis, and involvement of the ophthalmic division of the trigeminal nerve
145
What are some clinical manifestations of a meningioma originating from olfactory groove?
anosomia, personality change, and visual failure
146
What are some clinical manifestations of a meningioma originating from parasagittal region?
focal seizures of a focal motor or sensory deficit
147
What are some clinical manifestations of a meningioma originating from parasellar region?
evidence of chiasmatic compression; urinary incontinence; dementia; gradual paraparesis, hormonal failure; optic atrophy; bitemporal hemianopia
148
What are some clinical manifestations of a meningioma originating from lateral convexity region?
variable depending on structures compressed, including slow hemiparesis, speech abnormalities
149
What are nerve sheath tumors?
- either neurofibroma or schwannoma
| - inherited autosomal dominant disorder
150
What are the most common tumors to have brain metastases?
lung and breast
151
What is the metastatic cascade?
1. invasion of primary tumor border
2. extravasation of the circulatory system
3. survival and persistence/quiescence in the circulation
4. extravasation at the distant CNS site
5. Formation of micrometastasis
6. progressive colonization and growth
152
How are spinal tumors classified?
intramedullary - originating from tissues within the neural tissue
extramedullary - originating from tissues outside the spinal cord
153
What are the classifications of extramedullary spinal tumors?
intradural - arise from the meninges or roots
| extradural - epidural tissue or vertebral structure
154
Pathophysiology of intramedullary and extramedullary spinal tumors.
intramedullary - produce dysfunction by invasion and compression
extramedullary - produce dysfunction by compression of adjacent tissue, not by direct invasion
155
What are the clinical manifestations of spinal cord tumors?
compressive syndrome
irritative syndrom
syringomyelic syndrome
156
What is compressive syndrome?
associated with compression and is caused less frequently by invasion and destruction of spinal tracts
157
What is irritative syndrome?
combines clinical manifestations of a cord compression syndrome with radicular pain, which is pain in the sensory root distribution and indicates root irritation
158
What is syringomyelic syndrome?
inflammation of the spinal cord - results in the development of tubular (syrinx) cavities in the spinal cord
159
What is brown-sequard syndrome?
- associated with penetrating injuries, hyperextension and flexion, locked facets, and compression fractures
- ipsilateral paralysis or paresis below the level of injury
- ipsilateral loss of touch, pressure, vibration, and position sense below the injury
- contralateral loss of pain and temperature sensations below the level of the injury
160
What is anterior cord syndrome?
- compromise of anterior spinal artery
- loss of motor function below level of injury
- loss of pain and temperature sensations below the level of injury
- touch, pressure, position, and vibration intact
161
WHat is posterior cord syndrome?
-associated with hyperextension
| impaired light touch and propioception
162
What is conus medullaris syndrome?
- compression injury at T12
- flaccid paralysis of legs
- flaccid paralysis of anal spincter
- variable sensory deficits
163
What is cauda equina syndrome?
- compression of nerve roots below L1
- lower extremity motor deficits
- variable sensorimotor dysfunction
- variable reflex dysfunction
- variable bladder, bowl, and sexual dysfunction
164
What is horner syndrome?
- injury to preganglionic sympathetic trunk or postganglionic sympathetic neurons or superior cervical
- ipsilateral pupil smaller than contralateral pupil
- sunken ipsilateral eyeball
- ptosis of affected eyeball
- lack of perspiration on ipsilateral side of face
165
What is meningitis?
- infection of the meninges
- caused by bacteria, viruses, fungi, parasites, or other toxins
- classified as acute, subacute and chronic
166
Bacterial meningitis
- infection of pia mater and arachnoid, subarachnoid space, the ventricular system and the CSF
- caused by a systemic blood infection
- meningococcus and pneumococcus most common
167
What are clinical manifestations of bacterial meningitits?
- imflammation and irritation - headache, photophobia, nuchal rigidity, kernig sign, brudzinski sign
- local tissue dysfunction - cranial nerve palsy, seizures
- mass effect- n/v, increased ICP, decreased consciousness
- vascular compromise
168
How is bacterial meningitis treated?
appropriate bacteria and supportive therapies
169
What is aseptic meningitis?
- viral
| - inflammation limited to meninges
170
how is aseptic meningitis treated?
antivirals and steroids
171
What is fungal meningitis?
- chronic, much less common
- impaired immune system
- syphilis, TB, and lyme disease associated with it
- tx with antibiotics
172
What is tubercular meningitis ?
-most common and serious CNS TB
173
HIV-associated cognitive dysfunction
- typically later in the disease
| - HIV infected leukocytes adhere to endothelial lining
174
HIV myelopathy
- involving diffuse degeneration of the spinal cord
| - lateral and posterior columns of spinal cord affected
175
HIV neuropathy
- progressive radiculopathy of predominately dorsal roots of the lumbar and sacral nerves
- sensory, autonomic, mononeuritis multiplex, guillian-barre like syndrome, and myopathy
176
HIV- Aseptic viral meningitis
- headache, fever, meningismus
| - at time of seroconversion, represents the initial infection of the nervous system by HIV
177
Opportunistic infections
-may be bacterial, viral, protozoal or fungal
178
Cytomegalovirus infections
-common with AIDS however not diagnosed while the person is alive
179
Parasitic infection
- toxoplasmosis
| - produces a necrotizing process
180
CNS neoplasm
-CNA lymphoma, systemic non-Hodgkin lymphoma, metastatic kaposi sarcoma
181
Alzheimers Disease
- Familial, early and late onset
- Nonhereditary (sporadic, late onset)
- -Theories
- Mutation for encoding amyloid precursor protein
- Alteration in apolipoprotein E
- Pathologic activation of N-methyl-D-aspartate (NMDA)
182
Alzheimers Disease clinical manifestations
-Neurofibrillary tangles
-Senile plaques
-Forgetfulness, emotional upset, disorientation, confusion, lack of concentration, decline in abstraction, problem solving, and judgment
Insidious onset
-Diagnosis made by ruling out other causes of dementia
183
Parkinson Disease
Severe degeneration of the basal ganglia (corpus striatum) involving the dopaminergic nigrostriatal pathway
184
Parkinson Disease clinical manifestations
```
Parkinsonian rigidity
Parkinsonian bradykinesia
Parkinsonian tremor
Postural abnormalities
Autonomic and neuroendocrine symptoms
Cognitive-affective symptoms
```
185
Parkinson Disease and Dementia
- 50% of persons have depression, an inherent part of the pathologic state and not a situational response
- 30% treated on outpatient basis have dementia; 80% of persons requiring institutional care have dementia
- Disorientation, confusion, memory loss, distractibility, and difficulty with concept formation, abstraction, calculations, thinking, and judgment
186
Huntington Disease
- Also known as chorea
- Autosomal dominant hereditary-degenerative disorder
- Severe degeneration of the basal ganglia (caudate and putamen nuclei) and frontal cerebral cortex
- Depletion of gamma-aminobutyric acid (GABA)
- Choreiform movemets
- Disrupted thought processes
187
Multiple sclerosis (MS)
Progressive, inflammatory, demyelinating, autoimmune disorder of the CNS
Degeneration of the myelin sheath in CNS neurons
188
WHat are the different types of MS?
Mixed (general)
Spinal
Cerebellar
189
Amyotrophic lateral sclerosis (ALS)
- Classic ALS—Lou Gehrig’s disease
- Diffusely affects upper and lower motor neurons of the cerebral cortex, brainstem, and spinal cord (corticospinal tracts and anterior roots)
- Progressive weakness leading to respiratory failure and death
- Person has normal intellectual and sensory function until death
190
What are the different types of neuropathies
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Generalized symmetric polyneuropathies
Distal axonal polyneuropathy
Demyelinating polyneuropathy
Generalized neuropathies
Sensory neuropathies
Focal or multifocal neuropathies
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191
Guillain-Barré syndrome
- Acquired inflammatory disease causing demyelination of the peripheral nerves with relative sparing of axons
- Acute onset, ascending motor paralysis
- Humoral and cellular immunologic reaction
192
Myasthenia gravis
- Chronic autoimmune disease
- IgG antibody produced against acetylcholine receptors (antiacetylcholine receptor antibodies)
- Weakness and fatigue of muscles of the eyes and the throat, causing diplopia, difficulty chewing, talking, swallowing
193
What are the different classifications of MG?
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Neonatal myasthenia
Congenital myasthenia
Juvenile myasthenia
Ocular myasthenia
Generalized autoimmune myasthenia
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194
What is a myasthenic crisis?
severe muscles weakness causes extreme quadriparesis or quadriplegia, respiratory insufficiency; happens 3-4 hours after taking a medication
195
What is a cholingeric crisis?
resembles myasthenic crisis but weakness occurs 30-60mins after taking anticholinergic meds
196
Coma
- Bilateral hemisphere damage or suppression
| - Brainstem lesions or metabolic derangement that damages or suppresses the reticular activating system
197
What are a few clinical manifestations of a coma?
- Level of consciousness changes
- Pattern of breathing
- Posthyperventilation apnea (PHVA)
- Cheyne-Stokes respirations (CSR)
- Pupillary changes
- Oculomotor responses (Doll’s eyes)
- Motor responses
198
Brain Death (brainstem death)
-Body cannot maintain internal homeostasis
199
Brain death criteria
Completion of all appropriate, therapeutic procedures
Unresponsive coma (absence of motor and reflex responses)
No spontaneous respirations (apnea)
No cephalic (ocular or caloric) reflexes
Isoelectric EEG
Persistence for 1 hour and 6 hours after onset
200
Cerebral death
- Cerebral death (irreversible coma): death of the cerebral hemispheres exclusive of the brainstem and cerebellum
- No behavioral or environmental responses
- The brain can continue to maintain normal respiratory and cardiovascular functions, temperature control, and GI function
201
What are seizures?
- Disruption in balance of excitation and inhibition
- Sudden, transient alteration of brain function caused by an abrupt explosive, disorderly discharge of cerebral neurons
- Motor, sensory, autonomic, or psychic
202
What is a convulsion?
Tonic-clonic (jerky, contract-relax) movements associated with some seizures
203
What are the different classifications of seizures?
Generalized seizures
Partial (focal) seizures
Secondary generalization
Status epilepticus
204
What is status epilepticus?
Experience of a second seizure before the person has fully regained consciousness from the preceding seizure or a single seizure lasting more than 30 minutes
205
What are some seizure consequences?
- Available glucose and oxygen are depleted
- With severe seizures the brain tissue may require more ATP than can be produced
- Lactate accumulates in the brain tissues
- May produce secondary hypoxia, acidosis, and lactate accumulation
- May result in progressive brain tissue injury and destruction
- Cellular exhaustion and destruction
