Neuro Flashcards
(193 cards)
1
Q
Afferent
A
Toward the centre; e.g., afferent nerves carry impulses toward the central nervous system
2
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Amnesia
A
Loss of memory
3
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Anecephaly
A
Congenital condition where most of the brain and skull are absent
4
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Anomalies; Anomaly
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An abnormal structure, often congenital
5
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Aphasia
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Loss of the ability to communicate, speak coherently, or understand speech
6
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Athetoid
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Involuntary writhing movement of limbs and body
7
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Atresia
A
The absence of a canal or opening
8
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Aura
A
A sensation, e.g., visual or auditory, usually preceding a seizure or migraine headache
9
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Bifurcation
A
The division of a tube of a vessel into two channels or branches
10
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Choreiform (Chorea?)
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Involuntary repeated jerky movements of face and limbs
11
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Clonic Movements
A
Consisting of rapid, alternating contraction and relaxation of skeletal muscle
12
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Cognitive
A
Intellectual abilities, e.g., memory, thinking, problem solving, judgement, initiative
13
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Coma
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Unconscious state; person cannot be aroused
14
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Contralateral
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Opposite side of the body
15
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Disorientation
A
Mental confusion with inadequate or incorrect awareness of time, place, and person
16
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Efferent
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Moving away from the centre; e.g., efferent nerve fibbers carry motor impulses to muscles
17
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Fissure
A
A crack or split in the surface of skin or mucous membrane
18
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Flaccid (Flaccidity)
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Lack of tone in muscle; weakness and softness
19
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Foramina (Foramen)
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An opening in bone or membrane
20
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Fulminant
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Rapid, severe, uncontrolled progress of a disease or infection
21
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Ganglion
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A collection of nerve cell bodies, usually outside the central nervous system
22
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Gyri
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Elevations that cover the outer surface of the cerebral hemispheres
23
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Hyperreflexia
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Excessive reflex response
24
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Infratentorial
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A lesion located in the brain stem, or below the tentorium.
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Ipsilateral
Same side of the body
26
Labile
Unstable, changing
27
Nuchal Rigidity
A stiff neck, often associated with meningitis or brain hemorrhage
28
Paralysis
Loss or impairment of motor function in a part due to lesion of the neural or muscular mechanism
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Paresis
Muscle weakness or mild paralysis
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Paresthesia
Abnormal sensations
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Photophobia
Increased sensitivity of the eyes to light
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Postictal
Following a seizure
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Precursor
A substance that can be used to form other materials
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Pressoreceptors
Receptors in the vascular system, particularly in the aorta and carotid sinus, which are sensitive to stretch of the vessel walls
35
Prodromal
The initial period in the development of disease before acute symptoms occur
36
Ptosis
Drooping eyelid
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Retina
Light sensitive layer of the eye
38
Scotoma
A defect in the visual field
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Spastic
The nature of, or characterized by spasms
40
Stupor
A state of extreme lethargy, unawareness, and unresponsiveness
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Sulcus, Sulci
A groove or furrow, as one of the grooves on the surface of the cerebrum
42
Supratentorial
Denoting cranial contents located above the tentorium cerebelli
43
Sutures
Materials used in closing a surgical or traumatic wound
44
Tetraplegia
Paralysis of all four limbs; quadriplegia
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Tonic
Characterized by continuous tension
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Transillumination
The passage of light through a structure to determine if an abnormality is present
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Brain Function: Lobes
Frontal: Speech
Parietal: Speech, taste, hearing
Occipital: Vision
Temporal: Smell, hearing
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Support and Protection of the CNS
Cranium: Needs to stay closed
Meninges- Pia, Arachnoid, Dura
Cerebral Spinal Fluid (coats brain and spinal cord)
Vertebral Column (coats spinal nerves)
49
Headaches
May result from brain tumours, meningitis, head injuries, stress, muscle tension or a combination of factors
Can be acute or chronic
Caused by the stretching, dilation, inflammation and pressure of the pain sensitive structures within the cranium
50
Most common types of headaches are:
Migraine
Cluster
Tension
51
Migraine:
Familial, episodic disorder whose marker is headache and is defined as repeated, episodic headache lasting 4-72 hours
Usually women 25-55 yrs old (menstruation)
Caused by combination of multiple genetic and environmental factors
May have aura (physical/ psychological factors; smell burnt toast; "aura" to headache/ seizure)
52
Triggers (Seizures and migraines triggered by the same things):
```
Altered sleep patterns
Skipping meals
Overexertion
Weather change
Stress or relaxation from stress
Hormonal changes
Excess afferent stimulation (bright lights, strong smells)
Chemicals (alcohol or nitrates)
```
53
Migraine Diagnostic Studies
No specific laboratory or radiological tests
| Diagnosis is usually made from history
54
Cluster Headache
Characterized by repeated headaches that occur for weeks or months at a time, followed by periods of remission
One of the most severe forms of head pain
Occur less frequently than migraine
55
Cluster Headaches
More common in men 20-50
Severe unilateral pain, located around or behind an eye, can wake you up, may also have nasal congestion, tearing and facial flushing
Can be triggered by alcohol
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Cluster Headache: Etiology and Pathophysiology
Neither cause nor pathophysiological mechanism is known
Trigeminal nerve is implicated (runny nose, facial swelling)
Extracranial vasodilation occurs in affected part of face
57
Cluster Headache: Clinical Manifestations
```
Severe unilateral orbital, supraorbital, or temporal pain and at least one of the following:
Conjuctival injection
lacrimation
Nasal congestion
Rhinorrhea
Forehead and facial swelling
Miosis
Ptosis
Eyelid edema
```
58
Cluster Headache: Clinical Manifestations
Onset is abrupt, usually without prodrome (aura)
Peaks in 5-10 minutes and lasts 30-90 minutes (shorter than a migraine)
Common to start at night
Recur several times a day for several days
59
Cluster Headache: Clinical Manifestations
Affects upper face, periorbital region, and forehead on one side of the face and head
Partial Horner's syndrome may be seen
Described as deep, steady, and penetrating, but not throbbing
Client often paces floor, cries out, and resents being touched (become very sensitive)
60
Tension Headache
Most common
Average onset 2nd decade (men and women)
Occurs in episodes and may last for several hours or several days
Occurs at least 15 days per month for at least 3 months
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Tension Headache: Clinical Manifestations
No prodrome
Classification system lists tension-type as having a least two characteristics of:
Gradual onset
Pressure or tightness sensation, pain
Mild-moderate severity
Bilateral feeling of pressure around the head
Worsening with physical activity (musculoskeletal component)
May experience photophobia (light sensitivity) or phono phobia (sound sensitivity)
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Head Injuries
Major Head trauma: A rheumatic insult to the brain possibly producing physical, intellectual, emotional, social, and vocational changes
High potential for poor outcome
Majority of death occur at three points in time after injury: Immediately after the injury; within 2 hours after the injury; 3 weeks after injury
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Etiology of Head Injuries
Young adults: sports injuries; accidents (cars and motorcycles); violent assaults
Boxers or other athletes (contact sports)
Elderly (falls)
Infants (Shaken baby syndrome)
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Head Injuries:
```
May involve:
Skull fractures (break in the skull)
Scalp laceration (profuse bleeding; infection)
Concussion, contusion, and hematomas
Open or closed
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Head Injuries: Skull Fractures
Linear: Simple clean break in skull
Comminuted: Skull in fragmented pieces
Depressed: Skull bone fragments pushed into brain (infection, ischemia, necrosis)
Basilar: At base of skull, may extend to temporal bone
66
Basilar Skull Fracture: Manifestations
Can cause CSF or blood to leak from the nose (rhinorhea) or the ears (otorrhea)
Battle's sign (bruising mastoid)
Periorbital ecchymosis (raccoon eyes)
If CSF is leaking, risk for infection is high
67
Head Injuries Categories:
Mild concussion
Classical concussion
Mild, moderate, and severe diffuse axonal injuries (DAI)
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Concussion
A sudden transient mechanical head injury with disruption of neural activity and a change in LOC
Mild head trauma
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Concussion
Caused by violent shaking of the brain (rattling, shaking movement)
Immediate loss of consciousness
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Mild Concussion
Temporary axonal disturbance causing attention and memory deficits but no loss of consciousness
I: confusion, disorientation, and momentary amnesia
II: momentary confusion and retrograde amnesia
III: confusion with retrograde and anterograde amnesia (don't remember events before or after)
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Classic Cerebral Concussion
Grade IV
Disconnection of cerebral systems from the brain stem and reticular activating system
Physiologic and neurologic dysfunction without substantial anatomic disruption
Loss of consciousness (
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Open Head Injury : Through skull and dura
Injury breaks the dura and exposes the cranial contents to the environment
Causes primarily focal injuries
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Closed Head Injuries
```
The dura remains intact and brain tissues are not exposed to the environment
Head strikes hard surface or a rapidly moving object strikes the head
Causes focal (local) or diffuse (general) brain injuries
```
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Closed Head Injuries
Coup Injury: Injury directly below the point of impact
| Contrecoup: Injury on the point opposite the site of impact
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Closed Head Injury: Coup Contrecoup
Bruising of brain at two points
| Brain Damage: Focal symptoms related to area of brain injured; Possible increased ICP
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Diffuse Axonal Injury Etiology
Shaking, inertial effect
Acceleration/ deceleration
Axonal damage
Shearing, tearing, or stretching of nerve fibbers
Severity corresponds to the amount of shearing force applied to the brain and brain stem
77
Diffuse Axonal Injury: Clinical Signs
Decreased LOC
Increased ICP
Decerebration or decortication (signs that there is pressure on the brain stem)
Global cerebral edema
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Diffuse Axonal Injury
Produces a traumatic coma lasting more than 6 hours because of axonal disruption: Mild; Moderate; Severe
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Contusion
The bruising of brain tissue within a focal area that maintains the integrity of the pia mater and arachnoid layers
Major Head Trauma
80
Contusions
Observable brain lesion
Force of impact typically produces contusions
Can Cause: Extradural (epidural) hemorrhages or hematomas; Subdural hematomas; Intracerebral hematomas
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Contusion
Bruising/swelling of brain tissue caused by blunt trauma
Initial loss of consciousness with the following: Motionless, pale, clammy; Hypotensive, weak pulse, shallow respirations; Altered motor response
82
Epidural Hematoma
```
Arterial bleed (fast bleed) between skull and dura
Can be caused by skull fracture/ contusion causing tear in middle menigeal artery
Brief loss of consciousness short period of alertness rapid progression to coma with: Posturing (decorticate or decerebrate posturing, ipsilateral pupil changes, seizures
```
83
Subdural Hematoma
Venous bleed between dura and arachnoid layer
| Much slower to develop into a mass large enough to produce symptoms
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Aute Subdural Hematoma
Signs within 48 hours of the injury
Client appears drowsy and confused
Ipsilateral pupil dilates and becomes fixed
Rapid progression to coma, pupil dilation, contralateral hemiparesis
85
Subacute subdural hematoma
Occurs within 2-14 days of the injury
| Failure to regain consciousness may be an indicator
86
Subdural Hematoma: Chronic
```
Symptoms weeks to months later after a seemingly minor head injury
Impaired thinking
Confusion
Drowsiness
Pupil changes
Motor deficits
```
87
Subarachnoid Hemorrhage
Occurs in the space between the arachnoid and pia-subarachnoid space
Bleeding occurs from ruptured blood vessels, aneurysm or arterial venous malformation
Most occur in circle of Willis (perfusion centre for the brain)
Genetic component, women> men, >50
88
SAH Symptoms:
Cranial nerve deficits non reacting pupil, ptosis, altered LOC
Meningeal irritation - N/V, stiff neck, photophobia
Cerebral edema and increased ICP-seizure, hypertension, bradycardia, widening pulse pressure, diabetes insipidus
89
Intracerebral Hematoma
Bleeding into brain tissue
| May be caused by gunshot wound or a depressed skull fracture: Decreasing LOC, Pupil changes, Motor deficits
90
ICP
Skull has three essential components:
Brain tissue (80)
Blood (10)
Cerebrospinal fluid (10)
91
Intracranial Pressure: Factors that influence
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Arterial pressure
Venous pressure
Intra-abdominal and intrathoracic pressure
Body position (decrease/ pooling)
Temperature (^ metabolism; ^ ICP)
Blood gases (CO2 and O2 levels)
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The degree to which these factors ^ ICP depends on the ability of the brain to compensate for the changes
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Intracranial Pressure Regulation and Maintenance
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Normal compensatory adaptations:
Alteration of CSF production
Displacement of CSF into spinal subarachnoid space and other cisterns
Alterations in intracranial blood volume
Compression of brain tissue
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93
Mechanisms of Increased ICP
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Causes:
Mass lesion
Cerebral edema
Head Injury
Brain inflammation
Metabolic insult
```
Sustained increases in ICP result in brain tissue compression and may lead to life threatening herniation of the brain from one compartment to another
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Increased ICP: Clinical Manifestations
Papilledema
Headache (often continuous and worse in the evening when lying down; pressure and perfusion)
Vomitting (not preceded by nausea; projectile)
Changes in LOC
Changes in VS (Cushing triad):
Increased systolic BP
Bradycardia
Irregular respirations
Ocular signs
Decrease in motor function (decerebrate posturing (extensor; indicates more serious damage; decorticate posturing (flexor))
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Increased ICP Complications:
Two major complications of uncontrolled ^ ICP:
Inadequate cerebral perfusion
Cerebral herniation
96
Herniation Syndromes: Supratentorial herniation
Uncal: Uncus or hippocampal gyrus (or both) shifts from the middle fossa through the tenurial notch into the posterior fossa
Central: Downward shift of the diencephalon through the tenurial notch
Cingulate: Cingulate gyrus shifts under the flax cerebri
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Herniation Syndromes: Infratentorial herniation
Cerebellar tonsil shifts through foramen magnum
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Brain Death (Total Brain Death)
Body can no longer maintain internal homeostasis
Brain death criteria:
Completion of all appropriate and therapeutic procedures
Unresponsive coma (absence of motor and reflex responses)
No spontaneous respirations (apnea)
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Brain Death (Brain Stem Death)
Brain death criteria:
No ocular responses
Isoelectric EEG (flat)
Persistence 6-12 hours after onset (no medications on board)
100
Brain Death Clinical Manifestations
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Doll eyes (Eyes will go where you move the head)
Cold calorics (Ice water in ear; no response in brain dead person
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Cerebral death
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Cerebral death (irreversible coma) is death of the cerebral hemispheres exclusive of the brain stem and cerebellum
No behavioural or environmental responses
The brain can continue to maintain internal homeostasis
```
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Cerebral Death
Survivors of cerebral death:
Remain in coma
Emerge into a persistent vegetative state
Progress into a minimal conscious state (MCS)
Locked-in syndrome
103
Multiple Sclerosis
Chronic, progressive, degenerative disorder of the CNS characterized by disseminated demyelination of nerve fibres of the brain and spinal cord
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MS: Etiology and athophysiolog
Cause is unknown
Related to infectious, immunological environmental and genetic factors
Multiple genes confer susceptibility to MS
Characterized by chronic inflammation, demyelination, and gliosis in the CNS
Primary neuropathological condition is an autoimmune disease orchestrated by auto reactive T cells
Disease process consists of loss of myelin, disappearance of oligodendrocytes, and proliferation of astrocytes
Changes result in plaque formation with plaques scattered throughout the CNS
Initially the myelin sheaths of the neurone in the brain and spinal cord are attacked, but the nerve fibre is not affected
Client may complain of noticeable impairment of function
Myelin can regenerate, and symptoms disappear, resulting in a remission
Myelin can be replaced by glial scar tissue (permanent loss)
Nerve impulses slow down without myelin
With destruction of axons, impulses are totally blocked
Results in permanent loss of nerve function
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MS: Clinical Manifestations
Characterized by chronic, progressive deterioration in some. Remissions and exacerbations in others (How long you stay in the 2 stages determines what type you have
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MS: Clinical Courses
Remitting-Relapsing: Most common, clearly defined relapses with full recovery
Primary-progressive: Disease progression with no clear relapses
Secondary-progressive: Relapsing-remitting with minor remissions; disability accumulates
Progression-Relapsing: Progressive from onset with acute relapses, with or without recovery
107
MS: Clinical Manifestations
Vague symptoms occur intermittently over months and years
Disease may not be diagnosed until long after the onset of the first symptom
Common S&S include motor, sensory, cerebellar, and emotional problems (cognitive changes)
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MS: Clinical Manifestations (Motor)
Weakness or paralysis of limbs, trunk, and head
Diplopia
Scanning speech
Spasticity of muscles
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MS: Clinical Manifestations (Sensory)
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Numbness and tingling
Blurred vision
Vertigo and tinnitus
Decreased hearing
Chronic neuropathic pain
```
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MS: Clinical Manifestations (Cerebellar)
Nystagmus
Ataxia
Dysarthria
Dysphagia
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MS: Clinical Manifestations (Emotional)
Anger
Depression
Euphoria
112
MS: Other Manifestations (Bowel and bladder)
Constipation
Spastic bladder: small capacity for urine results in incontinence
Flaccid bladder: large capacity for urine and no sensation to urinate
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MS: Other Manifestations (Sexual dysfunction)
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Erectile dysfunction
Decreased libido
Difficulty with orgasmic response
Painful intercourse
Decreased lubrication
```
114
MS: Diagnostic Studies
Based primarily on history, clinical manifestations, and presence of multiple lesions over time measured by MRI
Certain laboratory tests are used as adjuncts to clinical exam
CSF analysis: Increase in oligoclonal immunoglobulin G
Contains a higher number of lymphocytes and monocytes
Evoked responses are often delayed because of decreased nerve conduction from the eye and ear to the brain
MRS may also be used to evaluate clients with MS
115
Seizure
Paroxysmal, uncontrolled electrical discharge of neurone in the brain that interrupts normal function
Often symptoms of underlying illness
Possible aetiology related to metabolic disturbances
116
Seizure
Possible aetiology related to extra cranial disorders: Heart; hypertension; lung; kidneys; liver; systemic lupus erythematosus; DM; septicemia
117
Epilepsy
A condition in which a person has spontaneously recurring seizures caused by an underlying chronic condition
118
Epilepsy: Etiology and Pathophysiology
In epilepsy abnormal neurons undergo spontaneous firing
Firing spread to adjacent or distant areas of the brain
If activity involves the whole brain, generalized seizure occurs
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Epilepsy: Clinical Manifestations
Determined by site of electrical disturbance
Generalized or partial classification
May progress through several phases
120
Seizures: Clinical Manifestations
Prodromal phase precedes seizure with signs or activity
Aural phase with sensory warning
Ictal phase with full seizure
Post-ictal phase with rest and recovery
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Generalized seizures: Clinical Manifestations
Characterized by bilateral synchronous epileptic discharges in the brain from seizure onset
No warning or aura as entire brain is affected
Loss of consciousness from seconds to minutes
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Tonic-Clonic seizures: Clinical Manifestations
```
Body stiffens (tonic) with subsequent jerking of extremities (clonic)
Postical phase
```
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Generalized Seizures: Clinical Manifestations
Typical absence seizures (petit mal)
Myoclonic seizure: single/ several jerks
Atypical absence: myoclonic jerks, automatisms with the staring spell
Myoclonic Atonic (drop attack): fall down
124
Partial Seizures: Clinical Manifestations
Partial seizures referred to as partial focal seizures
Begin in a specific region of the cortex
May be confined to one side of the brain and remain partial or focal in nature
May involve entire brain, cumulating in tonic-clonic seizure
125
Partial seizures: Simple partial/ Complex partial
Simple partial with elementary symptoms, no loss of consciousness >1 minute
Complex partial can involve behavioural, emotional, affective, and cognitive functions with discharge focus in temporal lobe
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Seizures: Clinical Manifestations
Psychosensory symptoms that may occur during complex partial:
Distortions of visual or auditory sensations
Vertigo
Alterations in memory
Alterations in thought processes
127
Seizures: Complications
Status epileptics is a state of constant seizure or a condition in which seizures recur in rapid succession without return to consciousness between seizures
Neurological emergency (hypoxia is a huge concern)
Can involve any type of seizure
Trauma during seizures can cause severe injury and death
Social stigma
Discrimination in employment and education
Driving sanctions
128
Seizure: Diagnostic Studies
```
PMH
EEG (do not need to be in seizure state)
CBC, serum chemistries, liver, and kidney function, UA to rule out metabolic disorders (prolactin levels will increase after seizure)
```
129
Infections: Meningitis
Inflammation of the meninges: brain and spinal cord
Bacterial (bigger concern)
Viral (short-lived; self-limiting)
Sets up an inflammatory response which increases production of CSF which leads to cerebral edema and IICP
130
Infections: Meningitis S&S
```
Positive Brudzinski's sign and Kernig's sign
Headache, photophobia, nuchal rigidity
High fever, N/V
Restlessness, confusion, seizures
Altered LOC
Signs of IICP
Altered vital signs
Petechial rash or extensive ecchymoses (meningococcal meningitis)
```
131
Infections: Meningitis Complications
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Seizures
Hydrocephalus
Cerebral infarction
Coma and death
Can leave residual effects such as visual deficits, deafness, cranial nerve palsies or hemiplagia
```
132
Infections: Encephalitis
Acute inflammation of white and fray matter: brain and spinal cord
Damage of nerve cells (cerebral edema, necrosis, localized hemorrhage
S&S similar to meningitis
Usually of viral origin (transmitted by ticks or mosquitoes)
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Infections: Encephalitis
Mild to serious infection which could be fatal
Edema and areas of necrosis may lead to localized hemorrhage
IICP develops, brain herniation unless untreated
High fever, headache, stiff neck, seizures, confusion, and disorientation
LOC deteriorates and the client becomes comatose
134
Infections: Brain Abscess
Collection of purulent material within the brain
Manifestations similar to meningitis
Caused by streptococci, staphylococci, pneumococci
135
Infections: Brain Abscess
Body tries to protect the rest of the brain by forming a capsule around the pus
Capsule enlarges and compresses nerves and brain tissue (edema and IICP)
Headache, fever, chills, malaise, N/V, and drowsiness, confusion, weakness on one side and seizures
136
Brain Infections: Diagnostic Tests
Lumbar puncture (need to see what's happening inside the brain)
Culture, sensitivity and Gram stain or CSF
Blood, urine, throat, and nasal cultures
CT, MRI, skull x-rays
137
Cerebral Palsy
A group of disorders marked by some degree of motor impairment
Caused by neonatal brain damage
Brain tissue is altered by malformation, mechanical trauma, hypoxia, hemorrhage, hypoglycaemia, hyperbilirubinemia or other
Damage occurs in different areas of the brain leading to multiple clinical manifestations
138
C.P: Manifestations
May be evident at birth or delayed
Classified based on area affected or the motor disability
THREE MAJOR GROUPS:
Spastic paralysis (motor cortex or pyramidal tracts)
Athetoid (Basal nuclei or extra pyramidal tracts)
Ataxic (Cerebellum)
139
C.P: Diagnostic Tests
Assessing infant's motor skills and looking carefully at the infant's medical history (checking for slow development, abnormal muscle tone, and unusual posture)
MRI, CT, ultrasounds to assess brain and possible cause
Reflex test - Moro reflex remains past 6 months in CP
Hand preference test - not usually seen for first 12 months but in CP one side usually stronger
140
Stroke
Stroke occurs when there is schema to a part of the brain that results in death of brain cells
141
Stroke: Etiology and Pathophysiology
Blood is supplied to the brain by two major pairs of afters: Internal carotid arteries; Vertebral arteries
If blood flow to the brain is totally interrupted; neurological metabolism is altered in 30 seconds, metabolism stops in 2 minutes, cellular death occurs in 4 minutes
142
Stroke Risk Factors (Nonmodifiable)
Age
Gender (men more than women)
Race (more in caucasian)
Heredity
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Stroke Risk Factors (Modifiable)
Hypertension, Obesity, Oral Contraceptive use, Physical inactivity, Sickle Cell disease, Smoking, Hyperlipidemia, Asymptomatic Carotid Stenosis, DM, Heart disease, A. Fib, Heavy alcohol consumption, Hypercoagulability
144
Stroke: Etiology and Pathophysiology
Around the core area of schema is a border zone of reduced blood flow where schema is potentially reversible
If adequate blood flow can be restored early (
145
Types of Stroke
Ischemic: Transient ("mini stroke", comes and goes), Thrombic, Embolic
Hemorrhagic
146
Transient Ischemic Attack: Etiology and Pathophysiology
TIA is a temporary focal loss of neurological function caused by schema
Most TIAs resolve within 3 hours
F- face
A- aphagia
S- slurred speech
T- time
147
Ischemic Stroke: Thrombotic Stroke
Thrombosis occurs in relation to injury to a blood vessel wall and formation of a blood clot
Result of thrombosis or narrowing of the blood vessel
Plaque causes a clot to form
Most common cause of stroke
148
Ischemic Stroke: Embolic Stroke
Occur when an embolus lodges in and occludes a cerebral artery
Results in infarction and edema of the area supplied by the involved vessel
Second most common cause of stroke
149
Hemorrhagic Stroke
Intracerebral Hemorrhage
Bleeding within the brain caused by a rupture of a vessel
Hypertension is the most important cause
Hemorrhage commonly occurs during periods of activity
150
Hemorrhagic Stroke: Manifestations
Neurological deficits, headache, N/V, decreased levels of consciousness, and hypertension
151
stroke: Clinical Manifestations
Motor activity, Elimination, Intellectual function, Spatial-perceptual alterations, Personality, Affect, Sensation, Communication
152
Stroke Deficits
Damage to left hemisphere:
Loss of logical thinking ability, analytical skills, other intellectual abilities, communication skills
Damage to right hemisphere:
Impairs appreciation of music and art, Causes behavioural problems, Spatial orientation and recognition of relationships may be deficient, Self-care deficits common
153
Stroke: Clinical Manifestations (Communication)
Dysphasia refers to difficulty related to the comprehension or use of language and is due to partial disruption or loss
Dysphasia can be classified as non-fluent or fluent
154
Asphasia
Expressive (Broca's area, left frontal lobe): Cannot speak or write fluently or appropriately
Receptive (Wernicke's area, left temporal love, prefrontal): Unable to understand written or spoken language
Global (Broca's and Wernicke's areas and connecting fivers): Cannot express self or comprehend others' language
155
Stroke: Clinical manifestations (Communication)
Many clients also experience dysarthria (disturbance in the muscular control of speech; affects mechanics of speech)
Impairments may involve pronunciation, articulation, and phonation
Dysarthria does not affect the eating of communication or the comprehension of language
156
Stroke: Clinical manifestations (Communication)
Agraphia: Impaired writing ability
Alexia: Impaired reading ability
Agnosia: Loss of recognition or association
Dysarthria: Difficult articulation
157
Stroke: Clinical Manifestations (Affect)
Clients who suffer a stroke may have difficulty controlling their emotions
Emotional responses may be exaggerated or unpredictable
158
Stroke: Clinical manifestations (Sensory-Perceptual Alterations)
```
Can alter sensation and perception of temperature, vibration, pain, pressure and proprioception
Agnosia
Apraxia
Homonymous hemianopia
Neglect syndrome
```
159
Stroke: Clinical Manifestations (Elimination)
Most problems with urinary and bowel elimination occur initially and are temporary
When a stroke affects one hemisphere of the brain, the prognosis for normal bladder function is excellent
160
Stroke: Diagnostic Studies
When symptoms of a stroke occur, diagnostic studies are done to: Confirm that it is a stroke; Identify the likely cause of the stroke
CT is the primary diagnostic test used after a stroke
Cerebral blood flow studies
Cardiac assessment (look for underlying problems)
Blood work (coagulation)
161
Spinal Cord Injury: Initial Injury
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Spinal cord injury can be due to:
Cord compression by bone displacement
Interruption of blood supply to cord
Traction from pulling on cord
Penetrating trauma can result in tearing and transection
```
162
Spinal Cord Injury: Classification
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Flexion
Hyperextension
Flexion-rotation (most unstable)
Extension-rotation
Compression
```
163
Spinal Cord Injury: Degree of Injury
Complete cord lesion: Total loss of sensory and motor function below level of lesion
Incomplete cord lesion: Mixed loss of voluntary motor activity and sensation. Leaves some tracts intact
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Spinal Cord Injury: Initial Injury
Primary injury: Initial mechanical disruption of axons asa result of fracture or dislocation
Secondary injury: Ongoing, progressive damage that occurs after initial injure due to ischemia and cellular death
24 hours or less: permanent damage may occur
Edema secondary to inflammatory response is harmful because of lack of space for tissue expansion
Resultant compression of cord and extension of edema above and below injure increases ischemic damage
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Spinal Shock
Characterized by:
Decreased reflexes
Loss of sensation
Flaccid paralysis below level of injury
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Stage One: Spinal Shock
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30-60 minutes post injury
Loss of reflex activity below injury
Bradycardia and hypotension
Loss of sweating and temp control
Bowel and bladder dysfunction
Flaccid paralysis
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Spinal Shock: Stage 2 (Recovery)
Gradual return of reflex activity below the level of injury
Hyperreflexia, spastic paralysis, sensory deficits and reflex or neurogenic bladder/bowel
Urinary incontinence and reflex defecation
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Neurogenic Shock
Loss of vasomotor tone characterized by: Hypotension, Bradycardia, Warm, dry extremities
Loss of sympathetic innervation: Peripheral vasodilation, venous pooling, decreased cardiac output
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Spinal Injury: Clinical Manifestations
Generally a direct result of trauma
Causes:
Cord compression, Ischemia, Edema (if it is an incomplete fracture, edema can make it complete), Possible cord transection
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Spinal Injury: Clinical Manifestations
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Immediate post-injury problems:
Maintaining a patent airway
Adequate ventilation
Adequate circulating blood volume
Preventing extension of cord damage
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Spinal Injury: Clinical Manifestations (Respiratory System)
Cervical injury above level of C4: Total loss of respiratory muscle function; Mechanical ventilation required
Below level of C4: Diaphragmatic breathing if phrenic nerve is functioning
Hypoventilation almost always occurs with diaphragmatic respirations
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Spinal Injury: Clinical Manifestations (Respiratory System)
Atelactasis
Pneumonia
Artificial airway
Neurogenic pulmonary edema
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Spinal Injury: Clinical Manifestations (Cardiovascular System)
Injury above level of T6 greatly decreases influence of sympathetic nervous system; Bradycardia, Peripheral vasodilation, Hypotension, Autonomic Dysreflexia
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Autonomic Dysreflexia
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Exaggerated sympathetic response with SCI at or above the T6 level
Impulse is blocked by the SCI
Hypertensive crisis (up to 300 mm Hg)
Pounding headache
Flushed diaphoretic above lesion
Cold, pale, dry below lesion
Goosebumps; anxiety
Possible CVA/ death
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Spinal Injury: Clinical Manifestations (Urinary System)
Urinary retention
Bladder distention
In-dwelling catheter
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Spinal Injury: Clinical Manifestations (GI System)
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Above level of T5:
Hypomotility
Paralytic ileus
Gastric distention
Stress ulcers
Intra-abdominal bleeding may occur
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Spinal Injury: Clinical Manifestations (GI System)
Neurogenic bowel (incontinent all the time); Less voluntary neurological control over bowel; Bowel is areflexic; Decreased sphincter tone
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Spinal Injury: Clinical Manifestations (Integumentary system)
Skin breakdown from lack of movement over bony prominences
| Pressure ulcers
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Spinal Injury: Clinical Manifestations (Thermoregulation)
Poikilothermism: Body temperature = room temperature; Due to interruption of SNS; Decreased ability to sweat or shiver
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Spinal Injury: Clinical Manifestations (Metabolic needs)
Nasogastric suctioning may lead to metabolic alkalosis
Decreased tissue perfusion may lead to acidosis
Loss of body weight common
*Protein loss, electrolyte imbalances
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Spinal Injury: Clinical Manifestations (Peripheral Vascular Problems)
DVT common problem
| Pulmonary embolism one of the leading causes of death in clients with spinal cord injuries
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Spinal Cord Injury: Diagnostic Studies
Complete spine films
X-Rays
CT scan
MRI
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Parkinson's Disease
Disease of basal ganglia characterized by:
Slowing down in the initiation and execution of movement
^ Muscle tone (become more rigid)
Tremor at rest (pill rolling; 1st manifestation)
Impaired postural reflexes (affects musculoskeletal)
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PD: Etiology and Pathophysiology
Pathological process involves degeneration of dopamine-producing neurone in substantial nigra of the midbrain
Disrupts dopamine-acetylcholine balance in basal ganglia
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{D: Clinical Manifestations
Tremor
Rigidity
Bradykinesia
Progression may involve only one side of the body initially
Beginning stages may involve only mild tremor, slight limp, or decreased arm swing
Later stages may have shuffling, propulsive gait with arms flexed, and loss of postural reflexes
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PD: Clinical Manifestations
Tremor:
More prominent at rest and is aggravated by emotional stress or ^ concentration
Described as "pill rolling" because thumb and forefinger appear to move in rotary fashion
*Stress causes it to occur more
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PD: Clinical Manifesations
Rigidity:
Rigidity is typified by a jerky quality when the joint is moved
Rigidity is similar to intermittent catches in the movement of a cogwheel
Inhibits the alternating contraction and relaxation in opposing muscle groups, thus slowing movement
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PD: Clinical Maifestations
Bradykinesia:
Slowing down in initiation and execution of movement
Evident in loss of automatic movements: Blinking, Swinging of arms while walking; Swallowing saliva, Self-expression with facial movement
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PD: Complications
Caused by progressive deterioration and loss of spontaneity of movement
Dysphagia can lead to malnutrition or aspiration
Debilitation may lead to pneumonia, urinary tract infections, and skin breakdown
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PD: Complications
Gait slows, and turning is difficult
Gait usually consists of rapid, short, shuffling mini-steps
Posture is with head and neck bent forward and legs completely flexed (this becomes fixed)
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PD: Complications
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Side effects from drugs, particularly levodopa, include:
Dyskinesias
Hallucinations
Orthostatic Hypotension
Weakness
Akinesia
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PD: Diagnostic Tests
No specific tests
Diagnosis based solely on history and clinical features
Firm diagnosis can be made when at least 2 of 3 characteristics of classic triad (tremor, rigidity, and bradykinesia) are present
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Dementia
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