intracranial disorders part 1 Flashcards

1
Q

Seizures

A

Paroxysmal, uncontrolled electrical discharge of neurons in brain, interrupting normal function
Can be a symptom of underlying illness
May accompany other disorders or occur spontaneously without apparent cause
Seizures resulting from metabolic disturbances or other extracranial disorders are not considered epilepsy if seizures cease when underlying condition is treated

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2
Q

metabolic seizure orgins

A

Metabolic Disturbances:
- Acidosis
- Electrolyte imbalances
- Hypoglycemia
- Hypoxemia
- Alcohol withdrawal
- Dehydration or water intoxication

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3
Q

extracranial seizure orgins

A

Extracranial disorders:
- Heart
- Hypertension
- Lung
- Kidneys
- Liver
- Systemic lupus erythematosus
- Diabetes mellitus
- Septicemia
- Febrile seizures

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4
Q

epilespy

A
  • Condition in which a person has spontaneously recurring seizures
  • Affects approximately 0.6% of Canadians
  • Higher incidence in those >60 years of age
  • Epilepsy is more prevalent in developing countries
  • Males are slightly more likely to develop epilepsy than females
  • 75% of seizure disorders are considered idiopathic
  • Role of heredity in seizure disorders is difficult to determine
  • Some families carry predisposition in the form of low threshold to seizure-producing stimuli such as trauma, disease or high fever
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5
Q

Epilepsy – Possible Causes

A
  • First 6 months of life - severe birth injury, congenital birth defects involving CNS, infections
  • From ages 2 to 20 - infections, trauma, genetic factors
  • Between ages 20 and 30 - structural lesions of the brain (trauma, tumour, vascular disease)
  • After 50 - Cerebrovascular lesions, brain tumours
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6
Q

Epilepsy - Pathophysiology

A
  • Abnormal neurons undergo spontaneous firing
  • Spreads to adjacent or distant areas of the brain
  • If activity involves whole brain, generalized seizure occurs
  • Brain glial cells provide support, nourishment and protection to neurons
  • Gliosis is a change in the glial cells due to CNS damage
  • Often area of brain from which epileptic activity arises is found to have gliosis
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7
Q

Seizures – Clinical Manifestations

A
  • Determined by site of electrical disturbance
  • Divided into two major classes: generalized and partial
  • May progress through several phases
  • Prodromal phase precedes seizure with signs or activity
  • Aural phase with sensory warning
  • Ictal phase with full seizure
  • Postictal phase with rest and recovery
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8
Q

Tonic-Clonic Seizures (Grand Mal)

A
  • Characterized by loss of consciousness and falling
  • Body stiffens with subsequent jerking of extremities
  • Cyanosis, excessive salivation, and tongue or cheek biting may occur
  • Postictal phase for tonic-clonic characterized by muscle soreness, fatigue; patient may sleep for hours
  • May not feel normal for days
  • No memory of seizure
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9
Q

Absence Seizures (Petit Mal)

A
  • Occurs only in children and rarely into adolescence
  • May cease or develop into another type
  • Typical symptom is staring spell for only a few seconds and usually goes unnoticed
  • Brief loss of consciousness
  • May occur up to 100 times/day if untreated
  • EEG demonstrates pattern unique to this type of seizure
  • Often precipitated by hyperventilation and flashing lights
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10
Q

Partial or Partial Focal Seizures

A
  • Caused by focal irritations
  • Begin in specific region of cortex
  • May be confined to one side of brain and remain partial or focal in nature
  • May involve entire brain, become tonic-clonic
  • Any tonic-clonic seizure preceded by aura or warning is a partial seizure that generalizes secondarily
  • Second generalized seizure may result in transient residual neurological deficit postictally (Todd’s paralysis – focal weakness in part or all of the body, usually subsides in 48 hours)
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11
Q

partial or partial focal seizures simple

A

Simple: simple motor or sensory phenomena with elementary symptoms with no loss of consciousness and lasting less than 1 minute

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12
Q

ppartial or partial focal seizures complex

A

Complex: involve behavioural, emotional, affective, and cognitive function:
- alteration in consciousness followed by period of postictal confusion
- commonly lip-smacking and automatisms
- distortions of visual or auditory sensations
- vertigo, alteration in memory and/or thought

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13
Q

epilespy complications

A
  • Social stigma, discrimination in employment/education and driving sanctions
  • Trauma during seizures can cause injury and death (falls, burns, MVA etc)
  • Status epilepticus is state of constant seizure or condition when seizures recur in rapid succession without return to consciousness between seizures, is a neurological emergency
  • Permanent brain damage can result
  • Can involve any type of seizure
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14
Q

epilespy diagnostics

A
  • Accurate, comprehensive description of seizures with patient’s health history
  • EEG – within 24 hours of seizure, not definitive as can have seizure disorder with normal EEG, no seizure disorder with abnormal EEG
  • CBC, serum chemistries, liver and kidney function, UA to rule out metabolic disorders
  • CT or MRI in new-onset seizure to rule out structural lesion
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15
Q

epilespy medical management

A
  • Drug therapy aimed at prevention
  • 70% of patients controlled with medication
  • Serum levels of medication should be monitored
  • Anti-seizure drugs should not be discontinued abruptly as this can precipitate seizures
  • Emergency drug – Diazepam (Valium)
  • Control drugs:
  • Older - Phenytoin (Dilantin), Carbamazepine (Tegretol), Depakene (Valproic acid)
  • Newer - Gabapentin (Neurontin), Lamotrigine (Lamictal), Levetiracetam (Keppra)
  • Surgical removal of epileptic focus to prevent spread of epileptic activity in brain
  • Removal of one lobe (usually temporal) or cortex, or separation of two hemispheres (corpus callosotomy)
  • Benefits of surgery include reduction or cessation in frequency of seizures
  • Vagal nerve stimulation
  • Biofeedback to control seizures
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16
Q

epilespy nusing management

A
  • Thorough assessment/health history and history of events leading up to seizure especially if non-chronic/singular/first event to help determine cause
  • Headaches, aura, mood or behavioural changes before seizure

Assessment/care during seizure (ictal phase):
- loss of consciousness, time length of seizure if possible, watch for abnormal respiratory rate or apnea/airway occlusion, note limb movement (tightening then jerking, limbs involved)
- support head, maintain patent airway, turn to side, loosen constrictive clothing, ease to floor

Assessment/care post seizure (post-ictal phase):
- bitten tongue/cheek, vital signs (HR, BP, RR, O2 sat), bowel/urinary incontinence, weakness, paralysis, orientation
- may require suctioning or oxygen after seizure
- assessment of level of understanding, memory of event

  • Instruct on importance of adherence to medication, not to adjust dose without physician
  • Monitor for therapeutic drug levels
  • Teach family members emergency management
  • Emotional support and identification of coping mechanisms
  • Medical alert bracelets
  • Referrals to agencies and organizations
17
Q

parkinson diseases (PD)

A
  • Degeneration of dopamine-producing neurons in substantia nigra of the midbrain
  • Disrupts dopamine-acetylcholine balance in basal ganglia
  • Dopamine is a neurotransmitter essential for normal functioning of the extrapyramidal motor system, including control of posture, support, and voluntary motion
  • Symptoms of PD do not occur until 80% of neurons in the substantia nigra are lost
  • Characterized by slowing down in the initiation and execution of movement, increased muscle tone, tremor at rest, gait disturbance
  • Diagnosis increases with age, with peak onset in the seventh decade
  • More common in men, ratio of 3:2
  • It is thought that PD is the result of a complex interplay between environmental factors and the genetic makeup of the individual
18
Q

PD causes

A
  • Encephalitis lethargica (type A encephalitis)
  • Symptoms have occurred after intoxication with a variety of chemicals (eg. carbon monoxide)
  • Can also be seen after use of illicit drugs, including amphetamines and methamphetamines
  • Hydrocephalus, hypoxia, infections, stroke, tumour, and trauma
19
Q

PD clinical manifestations

A
  • Onset is gradual and insidious
  • Classic triad of PD – tremor, rigidity, bradykinesia
  • Beginning stages may involve only mild tremor, slight limp, or ↓ arm swing
  • Later stages may have shuffling, propulsive gait with arms flexed, and loss of postural reflexes
  • None of these beginning manifestations alone is sufficient evidence for a diagnosis of the disease
20
Q

tremor in PD

A
  • Tremor is often the first sign
  • So minimal initially that only the patient may notice it
  • 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
  • Can affect handwriting, causing it to trail off
  • Can involve the diaphragm, tongue, lips, and jaw but rarely causes shaking of the head
21
Q

PD- rigity

A
  • Increased resistance to passive motion when limbs are moved through ROM
  • Typified by a jerky quality when the joint is moved
  • Caused by sustained muscle contraction and elicits the following - soreness, feeling tired and achy, pain in the head, upper body, spine, or legs
  • Inhibits the alternating contraction and relaxation in opposite muscle groups, thus slowing movement
22
Q

PD bradykinesia

A

Slowing down in initiation and execution of movement
Evident in loss of autonomic (involuntary) movements:
- blinking
- swinging of arms while walking
- swallowing of saliva
- self-expression with facial movements
Results in stooped posture, shuffling gait, masked face (deadpan), drooling of saliva

23
Q

PD complications

A
  • Non-motor symptoms – depression, anxiety, apathy, fatigue, flat affect, pain, constipation, impotence, short-term memory impairment
  • As disease progresses, complications increase - motor symptoms, weakness, akinesia
  • More severe neuropsychiatric problems, dementia occurs in 40% of patients
  • Dysphagia may result in malnutrition/aspiration
  • General debilitation - pneumonia, UTIs, skin breakdown
  • Orthostatic hypotension may occur – falls/injury
  • Sleep disorders are common and potentially severe
24
Q

PD diagnostics

A
  • No specific tests
  • Diagnosis based solely on history, clinical features
  • Firm diagnosis can be made when at least two of three characteristics of the classic triad (tremor, rigidity, and bradykinesia) are present
  • Ultimate confirmation of PD is a positive response to antiparkinsonian drugs
  • Ongoing research is using MRI to examine cognitive dysfunction in patients with PD
25
Q

PD- drug therapy

A
  • Dopamine receptor agonists (mimic effects of dopamine), Apomorphine, Pramipexole, used in early stages
  • Levodopa with carbidopa (Sinemet) is often the next drug used when moderate to severe symptoms develop
  • Anticholinergics, antihistamines, β-adrenergic blockers, Amantadine (antiviral), MAO-B inhibitors
  • Initially, only one drug typically used, as disease progresses, combination therapy often required
  • Excessive dopaminergic drugs can lead to paradoxical intoxication (arrhythmias, nausea/vomiting, anxiety, SOB)
26
Q

PD surgical therapy

A
  • Procedures aimed at relieving symptoms
  • Used in patients who are usually unresponsive to drug therapy or have developed severe motor complications
  • Deep brain stimulation (DPS) involves placing an electrode in the brain – shown to improve motor function, reduce dyskinesia, med usage
  • Transplantation of fetal neural tissue into the basal ganglia, provides dopamine producing cells – still experimental
27
Q

PD nursing mangemnet

A

Promote physical exercise to limit the consequences from decreased mobility
Promote a well-balanced diet
- need food that is easily chewed and swallowed
- adequate roughage to prevent constipation
* - small frequent meals to prevent fatigue, food cut into bite sized pieces, provide ample time to eat to avoid frustration
* - Levodopa can be impaired by protein and B6 ingestion
* - Problems secondary to bradykinesia can be alleviated by consciously thinking about stepping over a line on the floor and lifting toes when stepping
* Get out of a chair by using arms and placing the back legs on small blocks
* Remove rugs and excess furniture
* Simplify clothing from buttons and hooks
* Use elevated toilet seats
* Caregivers may also experience stress associated with disease progression (i.e., dementia)

28
Q

confusion

A
  • Mental state characterized by disorientation to person, place or time
  • Causes bewilderment, perplexity, lack of orderly thought and the inability to act decisively
  • Don’t expect specifics in a hospital (when you are on vacation, do you know the day, date?)
  • Keep safe, reorientation may be needed frequently
  • Patients may memorize answers, ask different questions from time to time
29
Q
A