Neurological: Conditions Flashcards

1
Q

Myasthenia Gravis

  • Cause
  • Signs and symptoms
  • Rx
A
  • Acquired autoimmune deficit ofacetylcholine receptor; characterized by the failure at the neuromuscularjunction due to blockage of acetylcholine receptors at the post-synapticmembrane
  • S/S: weakness and increased fatigueof facial muscles (often first shows up in eye muscles)- - Rx: Strengthening AFTER administrationof anti-acetylcholinesterase, fatigue mngmt
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2
Q

What causes Duchenne Muscular Dystrophy?

  • What is the function of dystrophin?
  • What happens to muscle tissue?
A

Duchenne Muscular Dystrophy (DMD) = disruption of dystrophin gene leading to muscle weakness accompanied by muscle hypertrophy (issue with mm CT, fat infiltration); CK levels high (necrotic mm)
o mutation in single gene on X chromsome –> fail to produce dystrophin protein (dystrophin links sarcolemma to actin) = mm cells replaced by fat and CT  progessive symmetric mm wasting
o normally diagnosed by 5, dead by ~20

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3
Q

How does DMD present?

  • What are the 2 key signs
  • What would be normal on a pulmonary function test/ what would be abnormal
A

Presentation:
- Key Signs: Gower’s sign (uses hands on leg to stand up) & Calf psuedohypertrophy
- prox mm weakness, pelvic girlde then shoulder; scoliosis
- waddling gait, toe walking, lordosis, freq falls, difficulty standing up and climbing stairs, lower IQ
- On pulmonary function test: Functional Residual Capacity should be normal
• TLC, vital capacity and FEV1 will be decreased

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4
Q

What are the PT goals and roles for the treatment on DMD

A

PT: work on strength, independence, advocate; keep body flexible, upright and mobile as possible

Goals of PT intervention for a child with DMD are to retard the development of contracture & muscle weakness, which could lead to functional limitations, and thus, disability. The PT would also play a role in determining the appropriate use of assistive devices that could help maintain the child’s mobility such as wheelchairs, walkers & orthoses

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5
Q

What is Amyotrophic lateral sclerosis (ALS) (Lou Gehrig’s) disease?

  • Peripheral or proximal onset of symptoms
  • What is spared?
  • End stage treatment?
A

A motor neuron disease and gradual deterioration of BOTH UMN and LMN (may have both flaccid and spastic paresis); M>F; stages 1-6
o Characterized by rapidly progressive weakness, muscle atrophy and fasciculations, muscle spasticity, difficulty speaking (dysarthria), difficulty swallowing (dysphagia), and decline in breathing ability.
o Amyotrophy = mm fiber atrophy; lateral= lateral column atrophy; sclerosis= harden/thickening of axons
o Starts peripherally, moves central, mm groups are affected asymmetrically; gradual involvement of all striated muscles, bulbar (oral motor) are major concern; progresses to paralysis w/o remission
o Sparing: sensory system, cognition, bowel and bladder, autonomic
o End stage Rx: help with resp difficulties (chest clearance), treat complications of immobility, symptom relief, facilitate mobility, patient comfort

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6
Q

What are signs and symptoms of ALS

A

o paresis in a single muscle group
o corresponding muscle groups are asymmetrically affected (patchy distribution)
o fasciculations (twitching)
o metabolic involvement of the skin (papery, fragile, cold)
o gradual involvement of striated muscle (bulbar = major concern)
o progress to permanent paralysis
o flaccidity + spasticity may co-exist
o selective sparing (no ocular or cardiac, urethral & anal sphincter)

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7
Q

What is Parkinsons disease?

- Possible causes?

A

Chronic neurodegenerative disease in basal ganglia, (M=F), leading to decreased dopamine produced by substantia nigra
o dopamine normally inhibits ACh
o without dopamine = excessive excitatory output

Possible causes:
o viral (infection = swelling of brain)
o genetic
o toxic (drugs)
o injury or focal ischemia = can cause PD-like symptoms
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8
Q

Signs and symptoms of Parkinsons disease;

  • What are the 4 hallmark signs?
  • What other symptoms may present
A
  • S/S (classic)
    o bradykinesia = slowness of movement, can result in freezing
    o resting tremor
    o rigidity = velocity independent resistance to passive stretch
    o postural instability
- S/S (other)
o loss of automatic movement (ie rolling over in bed)
o micrographia
o autonomic abnormalities
o hypokinesia/akinesia
o mask face
o depression, dementia
o postural hypotension
o pain
o sleep disturbance (restless leg)
o fatigue
o decreased fine motor control
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9
Q

What is the pharmacological management and physiotherapy treatment for PD?

A

Pharmacological
o Levadopa (Sinemet)
 Prolonged use can lead to dyskinesias, GI disturbances, restlessness, anxiety, depression
o Selegiline: used in early PD
 Adverse effects: nausea, dry mouth, dizziness, anxiety, hallucinations

Physiotherapy
- education (protective effects of exercise)
- functional mobility exercise = FOCUS ON BIG MOVEMENTS
- cueing (tactile, verbal, music)
- Rx for festinating gait: use toe wedge to help displace COG backwards
- address postural changes and cardiorespiratory fitness
- transfers, balance and falls prevention
o prevention of secondary sequelae
o environment safety and checks
o care giver involvement and training
o equipment

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10
Q

What is Huntington’s chorea?

  • What causes abnormal movements
  • Physiotherapy treatment?
A

– Progressive, hereditary condition characterized by abnormal movement and mental deterioration; movement is purposeless, involuntary, brief and random; writhing (choreoform) movements including limbs, speech (sound drunk) due to loss of neurotransmitters and GABA
o PT Tx: symptom management, patient safety, maintain enough nutrition

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11
Q

Differentiare between;

  • Essential tremor
  • Dystonia
  • Hemiballismus
  • Tardive dyskinesia
  • Tourettes syndrome
  • Korsokoff syndrome
A

 Essential Tremor: common neurological disorder usually seen as shaking hands evoked by voluntary movements; no other neurologic signs; most frequently seen movement disorder
o Increases with fatigue/nervousness
 Dystonia: involuntary, sustained muscle contractions that produce repetitive movements and distorted or abnormal postures; may be action specific or linked to repetitive action
o Tx: adjust movement-related nerve signals, temporarily immobilize target muscles
 Hemiballism: exhaustingm violent movements; often resolves in 6-12 months
 Tardive Dyskinesia: motor control disorder secondary to use of neuroleptics for control of psychosis; random movements in tongue, lips, jaw
 Tourettes Syndrome: repetitive, involuntary, stereotypical movements and utterances (tics)
 Korsokoff’s syndrome = genetic metabolic injury due to malnutrition or alcoholism, can’t make new memories, characterized by confabulation; distored memories about one’s self or the world

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12
Q

What is multiple schlerosis?

  • What is the typical age onset
  • Cause
  • What are the signs and symptoms
A

o Multiple Sclerosis = an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged, leading to demyelination and scarring; unpredictable, chronic, debilitating
o Typical onset 20-40yo; NO known cause; HLA-DR2 may be genetic link
o S&S’s: fatigue, mm weakness, paraesthesia, optic neuritis or diplopia, vertigo, bowel and bladder, impaired cognition/memory, pain, depression

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13
Q

Differentiate between the different types of MS

A

o Types:

  • Relapsing remitting – new symptoms or old symptoms may resurface or worse and it can be full or partial recovery relapses can be days weeks or months recovery can be slow or instantaneous
  • Primary progressive- there is a gradual worsening of symptoms overtime may stabilize but no remission
  • Secondary progressive – starts off as relapsing remitting then steadily worsens
  • Progressive relapsing - there is a steady progression with attacks
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14
Q

What is the physiotherapy treatment for MS

  • Treatment considerations
  • Contraindication and precautions to exercise
A

o PT Rx: treat vestibular dysfunction, posture, proprioception, core, stretches, exercise will benefit overall fxn
o Rx program: late morning sessions, aggressive stretching, moderate exercise, energy conservation and stress management techniques
o Contraindications and precautions to exercise: heat, fatigue, pregnancy
- 80% of pts experience increase in neurological S&S with incr in heat

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15
Q

What is meningitis?

  • What is there an increased risk of?
  • Presentation of symtpoms (time frames)
  • Physical tests for meningitis?
A

 Meningitis: infectious disease that causes inflammation of meninges (all 3: pia, arachnoid, dura)

o Info: increased risk of infarctions, cortical veins may develop thomboses, may be block of CSF secondary to scar tissue (can cause hydrocephaly - excess amount of fluid in the brain) which causes headache (the CARDINAL SIGN!)

o Presentation: can present as acute (hrs-days); sub acute (2wks plus); chronic (1mo plus)

o Physical test for meningitis: patient supine, passively flex neck
- Brudzinski’s sign: knees and hips will flex

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16
Q

Treatment considerations for meningitis?

A

Tx considerations: Avoid undue oblique stress on any bone, maintain activities below the point of fatigue, elevate the patient toward vertical position slowly

o antibiotic (if bacterial)
o viral (control of symptoms)
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17
Q

What are the 3 main types of meningitis

A

Types:

1) aseptic (fungus, virus, parasite, can also get with: herpes syplex 2, ebstien barr, lupus)
2) tuberculosis: abcess or edema
3) bacterial: in child or infant is considered a medical emergency
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18
Q

What is encephalitis?

  • Signs and symptoms
  • What are the tests for meningitis and encephalitis?
A

Encephalitis: infection of the brain and SC
o S&S: headache, nausea, vomiting, LOC, coma can last for weeks; can result in focal brain damage

Investigations = EEG, CSF tap, MRI

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19
Q

What is lyme disease?

  • What are the 3 stages of presentation
  • What other syndromes and diseases can lyme disease mimic
A

Lyme disease: from a bacteria, Borrelia burgdorferi, through ticks
May occur in stages;
stage 1) localized presentation, erythema, flu like
stage 2) neuro (headache and neck stiffness) MSK and cardiac (tachy, brady, arrythmia, myocarditis) , may have Bells palsy
stage 3) final stage long term neuro, with arthritis (1/3) and cognitive deficits

o Info: mimics other diseases like MS, fibromyalgia, chronic fatigue syndrome, guillan barre

20
Q

What is the treatment for Lyme disease

A

Rx: antibiotics to treat infection

PT management: relieve pain, prep deconditioned patients for home ex, ed re FITT w/out exacerbating symptoms, improve strength

21
Q

What is Gullian Barre Syndrome (GBS)?

  • Cause
  • Signs and syndrome
A

Antibody mediated demyelination of Schwann cells in PNS from spinal nerves –> terminating fibres
- May be in hospital for 6-8 mo

Causes

  • immune disorder
  • 2/3 ppl had recent illness in last 30 days (flu vaccine)

S/S

  • onset to peak 4 weeks
  • rapid ascending SYMMETRICAL motor weakness and distal sensory loss –> spreads to arms, trunk, and face
  • stocking and glove pattern of loss*
  • absent DTR
  • may require mechanical ventilation
UON S&S
= Ascending paralysis
- Symmetrical flaccid tetraparesis
= Respiratory, trunk & eye muscles affected
= Facial & bulbar involvement
= Mild - minimal sensory loss
= Low back pain common
= Autonomic involvement
22
Q

What is the treatment for GBS?

A

RX
MEDICAL = Plasmaphoresis, immunoglobin
Antibiotics as > ½ develop chest infections

PT:

  • joint protection
  • chest rx, mobilization
  • strength
  • ROM (usually opposite to ALS progression)

UON PT intervention
􀂄 Observation of patient function, movement and pattern of paralysis, muscle bulk
􀂄 Muscle power; reflexes; fasciculations
􀂄 Functional ability and missing components
􀂄 Joint range / contracture
􀂄 Sensation / Pain; chart pattern and type of loss
􀂄 Autonomic symptoms eg BP, HR, body temp.
􀂄 Respiratory function
􀂄 Cranial nerve function (incl. Swallowing)

23
Q

What is CREUTZFELDT JAKOB DISEASE?

A
  • movement disorder/dementia  rapidly progressive + fatal
  • occurs in young adults

Pathology

  • caused by prions (misfolding proteins) –> bovine spongiform encephalopathy (mad cow disease)
  • contracted by ingestion or via the nose
  • incubates 5-8yrs
  • cannot make final Dx until death*
24
Q

What is post-polio syndrome (PPS)?

A

Attacks neurons in brainstem + anterior horn cells (spinal cord)

INITIAL EFFECT = death of motor neurons controlling skeletal muscles. Those that survive sprout new nerve terminals to make up for loss
RESULT = some mov’t recovery + enlarged motor units

After years of use = high metabolic stress on larger motor units is more than neuron can handle
RESULT = gradual deterioration of sprouted fibers & eventually neuron

MUSCLE WEAKNESS + PARALYSIS

25
Q

What is the general exercise guidlines for PPS

A

EXS PROGRAM: general body conditioning, balance period of rest & activity, do not ex. to point of fatigue, exs when less fatigued or most rested

26
Q

What can be some difficulties that can arise when strength testing someone w/ PPS

A

STRENGTH TESTING DIFFICULTIES: Strength varies with time of day tested and more likely to demonstrate fatigue and weakness in afternoon, fatigue with repeated testing and client may have learned to substitute or compensate for weaker groups

27
Q

What is the pathophysiology of GBS?

A
  1. Conduction block flaccid paralysis
  2. Recovery with regeneration, reinnervation
    and remyelination
  3. Severe GBS - secondary axonal degeneration
    slower recovery and increased residual
    disability
28
Q

What is the time frame for disease progressions and recovery for GBS

  • What are the 3 phases?
  • Time to lowest level of deterioration?
  • When does imrpovement start?
  • What is the median time to walk unaided?
  • Wen will most patients be able to ambulate?
A

10% die, 20% left severely disabled,10%
moderately disabled
3 phases : deterioration - plateau - recovery

Time to lowest level of deterioration:
50% - 1 week
70% - 2 weeks
100% - 4 weeks

Improvement – most within 8 weeks
Median time to walk unaided – 3 months
80% ambulant by 6 months

29
Q

What are the cardinal signs of cerebellar ataxia

A
  • Hypotonia
  • Ataxia
  • Dysarthria
  • Tremor
  • Ocular Motor Dysfunction
30
Q

What is the function and deficit of Vestibulocerebellum

Archicerebellum

A

EQUILIBRIUM & EYE MOVEMENTS
Flocculonodular

For balance
= postural instability during stance and gait (postural sway & trunkal ataxia)
= decreased postural reflexes
= nausea

For coordinating eye & head mvts
= Vestibulo-ocular reflex (VOR)
= Cerebellar nystagmus (can mimic vestibular disease)

31
Q

What is the function and deficit of the Spinocerebellum

Paleocerebellum

A

POSTURAL TONE & MOTOR EXECUTION
REGULATING MOTOR PERFORMANCE
Anterior lobe

Linked to hypotonia
- decreased excitation of alpha and gamma motor
neurons
- more noticebale in the UL’s and proximal mms
- usually accompanies acute lesions

Loss of programmed deceleration leads to:

  • Hypermetria
  • Rebound phenomenon
  • Lack of motor plasticity or learning
  • Involvement of the legs resulting in gait ataxia
  • Intention tremour: As arm approaches target, goes into oscillations
32
Q

What is the function and deficit of the Neocerebellum

A

PLANNING & INITIATION OF MOVEMENT
VISUAL GUIDANCE OF MOVEMENT
Posterior lobe

Damage leads to:
- Movement decomposition: Difficulty performing a movement
in one smooth pattern and instead perform the movement in a
sequence of steps
- Asthenia
- Dysmetria
- Dysdiadochokinesia
- Delayed initiation of movements
- Dysarthria: scanning, slurred, staccato,hesitant, garbled
- Dyssynergy- a slow onset in development of muscle tension, reduced
intensity and slow release compared to normal movement; defective
timing of sequential contraction of agonist/antagonist mms
- There is a loss of anticipatory movements in response to perturbations
- Inability to adjust to environmental or specific task demands
- Problems with visual pursuit movements (occular dysmetria)

33
Q

What is Charcot Marie Tooth Disease?

- How does it present?

A

A hereditary motor and sensory neuropathology causing extensive demyelination of motor and sensory nerves, esp in feet;

Presentation- slow progression of symmetric mm weakness, atrophy of foot intrinsics, diminished deep tendon reflexes, pes cavus/hammer toes, weak dorsiflexors and pronators

UON
- Starts distally in lower limbs, spreads to distal
upper limbs: progressive wasting & sensory
loss, hyporeflexia
- Rarely: respiratory mm weakness, tremour
- Late in disease: joint deformity and
contractures

34
Q

What is the physiotherapy role is treatment on CMT

A

PT Rx: contracture management (stretching mm), management/education on foot care

35
Q

What is Bell’s Palsy?

  • What is the clinical presentation?
  • What nerve is involved and what does it innervate ?
  • What is the role of physiotherapy?
A

Bell’s Palsy = peripheral nerve injury of facial nerve where the motor nerves are injured while they pass through parotid gland; compression occurs when surrounding CT tissue is inflamed; d/t latent herpes virus; days before onset pt reports pain around mastoid; virus causes inflam response over facial nerve

Clinical manifestations- unilateral facial paralysis (getting drooping of corner of eye and mouth, “crocodile tear” and drooling)

Facial nn innervates -mm of facial expression, stapedius mm of inner ear, sensory and autonomic fibers for taste (ant aspect of tongue), tears, salivation

Rx: corticosteroids, estim?, protect eye (can dry out)

36
Q

What is diabetic neuropathy?

  • What is the pathology?
  • Hw does it present?
  • What is the role of physiotherapy?
A

Diabetic neuropathy = peripheral nn disorder in diabetes that occurs w/o any other cause for neuropathy

Pathology- chronic metabolic disturbance affects nn and schwann cells; hyperglycemia leads to abnormal micro-circulation = loss of both myelinated and unmyelinated axons

Presentation- symmetric, distal pattern of sensory loss, painless paraesthesia with MINIMAL motor weakness

Rx: control hyperglycemia, skin care, amputation is common d/t diabetic ulcers

37
Q

What is Complex Regional Pain Syndrome (CRPS)?

- What are the typical features?

A

A chronic pain condition believed to be the result of dysfx in central or peripheral NS; develops after trauma, Sx, UMNL

Typical features: changes in the color and temp of the skin over the affected limb or body part, with intense burning pain, skin sensitivity, sweating, swelling, stiffness

38
Q

What are the stages of Complex Regional Pain Syndrome (CRPS)

A

Stages:
 Stage 1 (0-3 mo): puffy swelling, redness, warmth, stiffness, allodynia, pos bone scan
• Do not use manipulation; use cold
 Stage 2 (3-6 mo): incrd P and stiffness, firm edema, cyanosis, atrophy, osteopenia on xray
• Use heat
 Stage 3 (6mo plus): tight, smooth, glossy, cool, pale skin; stiffness and contractures, nail and hair changes; severe osteopenia

39
Q

What is the role of physiotherapy for Complex Regional Pain Syndrome (CRPS)

A

PT Rx: prevention and early detection = early pain-free AROM and use, pain and edema mngmt (desensitization, contrast baths, modalities, TENS, gentle massage, electrical stimulation), education; NO PROM

40
Q

Differentiate between

  • Neuropraxia
  • Axonotmesis
  • Neuronotmesis
A

NEUROPRAXIA – compression of axon without severing the axon or sheath; causes a transient disruption
- Rapid and complete recovery (could take minutes to weeks)

AXONOTEMESIS – compression and severing of the axon (myelin sheath is still intact); may cause paralysis of the motor, sensory, and autonomic. Mainly seen in crush injury
- Slow recovery, 1-3 mm/day from point of injury; fair prognosis which can take months

NEUROTEMESIS – compression and complete severing of both the axon and sheath
- Recovery is only possible with surgery with variable success (i.e. it may never recover); Need surgical nerve transplant

41
Q

What is Cerebral palsy?

  • What are some secondary complications d/t CP?
  • What are the risk factors?
A

Non progressive lesion of the brain that occurs before the age of 2, resulting in hearing and speech problems, hydroencephalus, microencephaly, scoliosis, hip dislocation, mental retardation

Any prenatal, perinatal or postnatal condition that results in Anoxia, haemorrhage (intraventricular, periventricular leukomalacia - most common ishcemic brain injury in premature babies) or brain damage

Risk factors: older mom, low birth wt/small for gestational age, IVF (invitro fertilization), abnormal placenta attachment, blood type incompatability, Prematurity, low apgar score, anoxia

42
Q

Differentiate between the different physiological types of Cerebal Palsy

A

PHYSIOLOGICAL TYPES:
Spastic
- Mm stiffness, dec ROM, movements limited to synergies (primitive movement patterns), trouble start/stop movement
- May walk with scissors gait pattern
- Moderate spastic diplegia - CI to use bilateral KAFOs b/c extensor tone can provide antigravity support

Ataxic

  • Abnormal rate, range, force, duration of movements
  • Difficulty with rapid move, gait, fine motor, balance

Athetoid

  • Movement disorder d/t damage to basal ganglia. Characterized by both hyper- and hypo-tonia and uncontrolled movements of extremities and trunk
  • Slow twisting wide amplitude movements, changing of mouth positions
  • Lack of co-contraction of mucles leads to postural instability

Dystonic

  • Long sustained involuntary movements and postures
  • Tend to lock jts at end range; mid range control is difficult

Hypotonic
- Lack of tone, weakness

43
Q

Hip subluxation in CP

  • What mms contribute to dislocations?
  • What behavioural feature creates the most risk
  • First indication of instability at hip?
  • Treatment
A

Spasticity of adductor longus and iliopsoas, dislocate posteriorly
o Non-ambulatory child is most at risk
o First indication is inability to abduct >45deg

o Tx: seating, botox to adductors, surgery, baclofen pump, tendon release,
o Sitting modifications: put pummel between legs

44
Q

What is Spina Bifida?

- Differentiate between the different types

A

Neural tube defect = RESULT: vertebral and/or spinal cord malformation

  • Spina Bifida Occulta - no spinal cord involvement, may be indicated by hair tuft
  • Spina Bifida Cystica - visible or open lesion
  • Meningocele - cyst includes cerebrospinal fluid cord intact
  • Myelomeningocele - cyst includes CSF and herniated cord tissue

link between maternal decreased folic acid + infection + exposure to teratogens (alcohol)

45
Q

What are the signs and symptoms of Spina Bifida?

A
S/S
o flaccid or spastic muscles
o muscle weakness
o contractures
o muscle wasting
o dec/absent DTR
o rectal/bladder incontinence
o hydrocephalus (chiara malformation)
o osteoporosis, lordosis, scoliosis, kyphosis
o foot deformities  talipes equinovarus (club foot) esp with L4, L5 level
46
Q

What is the role of physiotherapy in the treatment of Spina Bifida?

A

RX
o ROM, strengthen functional muscles
o teach transfers
o equipment (orthodics, early mob, standing and ambulation)
o encourage awareness of sensory deficits (protection of feet, position of legs, check for sores)

47
Q

Differentiate between the different types of seizures?

A

TYPES

1) primary generalized seizures - bilateral and symmetrical w/out local onset
* Tonic-clonic (grand mal)
- dramatic, whole body - 2-5 mins

  • Absence seizures (petit mal)
  • brief, almost imperceptible LOC
  • come back to full consciousness
  • no change in posture
  • can be up to 100/day

2) partial seizures
* Simple partial seizure - usually one part of the body
- focal motor = clonic activity on specific area of body
- focal motor with march (Jacksonian) = orderly spread or march of clonic movements; can progress to whole side
- temporal lobe seizure = episodic change in behavior, complex hallucinations,

*Complex partial seizure - simple partial seizures followed by impairment of consciousness