Neuro Flashcards
Brainstem involvement
Ipsilateral facial impairments
contralateral trunk and limb impairments
Brain involvment
Cirtical lesion: Impairment is dependent on the location of somatosensory cortex affected
deeper lesions impacting the thalamus and adjacent structures can lead to diffuse unilateral dysfunction
Contralateral side affected (tracts cross)
superficial sensations
Light touch
pinprick (pain)
hot and cold
pressure
Deep sensations
kinesthesia
proprioception
vibraation
Combined sensations
stereognosis, tactile localization, two point discrimination, double simultaneous stimulation, graphesthesia, recognition of texture, barognosis
Sensory impairment terms Allodynia Analgesia Causalgia dysesthesia hyperalgesia hyperasthesia hypoalgesia paresthesia
Allodynia: Non-noxious stimulus produces pain
Analgesia: Loss of pain sensitivity (Inability to feel pain)
Causalgia: Burning painful sensation ( often along a nerve distribution)
dysesthesia: Touch sensation produces pain
hyperalgesia: Heightened sensitivity to pain
hyperasthesia: Heightened sensity to sensory stimulus
hypoalgesia: Decreased sensitivity to pain
paresthesia: Abnormal sensation with no apparent cause (Numbness, tingling)
UMN and LMN lesions
UMN Weakness (spastic paralysis), hyperreflexia, hypertonia
LMN (Weakness (Flaccid paralysis), atrophy, fasiculations, hyporeflexia, hypotonia)
UMN conditions
Traumatic brain injury (concussion) Stroke Cerbral Palsy Ataxia (Cerebellar ataxia) Spinal cord injuries Multiple Sclerosis Brain or spinal tumor
LMN conditions
Guillain barre syndrome Post polio poliomyelitis Bells Palsy ( Affects facial nerve) Cauda equina syndrome Peripheral nerve injuries
Which condition has S & S of both UMN and LMN lesions
ALS
Hypertonia: Rigidity (leadpipe and cogwheel) Are most common with what condition
Leadpipe rigidity (Uniform rigidity through range) Cogwheel rigidity (Rachet-like jerkiness through range Both common in parkinsons disease
Decorticate rigidity
Corticospinal tract lesion at level of diencephalon (Likely to be in a comma)
- Abnormal flexor response
- Upper extremities:
- Shoulder adduction
- Elbow flexion
- Wrist flexion
- Finger flexion
Lower extremities:
- leg extension and internally rotated
- Plantar flexion
Decerebrate rigidity
Corticospinal tract lesion at the level of the brainstem Abnormal extensor response UE: -Shoulder adduction -pronation -Elbow extension -Wrist flex -Finger flex LE: -Leg extended -Plantar flexed
Dystonia
Movement disorder characterized by involuntary twisting and repetitive movements, abnormal fixed postures, and disordered tone
Ischemic stroke
Most common form of stroke (80%)
thrombus (Most common) or an embolus that blocks an artery
TIA (Typically resolve in 24 hours) but administer thrombolytic agent within 4.5. hours
Hemmorhagic stroke
~20%
Increased mortality rate
Intracerebral (Rupture or leak of a weak blood vessel in the brain )
Subarachnoid ( Due to an arteriovenous malformation or a ruptured aneurysm which causes bleeding in the subarachnoid space)
Risk factors for stroke
Hypertension Heart disease Disorders of heaert rhythm Diabetes Hypercholesteremia (> 240 mg/dl) High LDL Low HDL Elevated hematocrit End stage renal disease sleep apnea
Major risk facxtors specific to women
Early menmopause
estrogen supplementation
Pregnancy, birth, first 6-weeks post partum
Preeclampsia
Modifiable and non-modifiable risk factors for stroke
Modifiable
- Smoking
- Physical activity
- Obesity
- Diet
- excessive alcohol use
Non-modifiable
- Family Hx
- sex (M>F)
- Age
- Race (African American)
Anterior cerebral artery syndrome (stroke)
If occlusion is proximal to the anterior communicating artery there will be minimal deficits
If distal then there will be greater deficits
Characteristics
- Contralateral hemiparesis and hemi-sensory loss
- LE>UE
- Urinary incontinence
- Abulia (absence of will power)
- Akinetic mutism (Decrease moving and speaking)
- Apraxia ( Difficulty with motor planning and movement)
- Broca-s apashia (frontal lobeO Motor speech impairment)
MCA syndrome
Supplies lateral aspect of cerebral hemisphere (Frontal, temporal, and parietal lobes) and subcortical structures (internal capsule, corona radiate, globus pallidus, caudate, and the putamen)
- Most common site of a stroke
- S & S
- Contralateral hemiparesis and hemi-sensory loss of face, UE, and LE
- UE affected>LE
- Contralateral HH
- werneickes aphasia
- Brocas aphasia
- Global aphasia (nonfluent speech and poor comprehension)
- Perceptual deficits (unilateral neglect, anosognosia, apraxia, spatial disorganization/depth perception) typically in the non-dominant right hemisphere so the deficits will be in the right
posterior carotid artery syndrome
PCA supplies the occipital lobe, medial and inferior temporal lobe, upper brainstem (midbrain), posterior diencephalon (includesmost of the thalamus)
common characteristics
-peripheral territory: amnesia (loss of memories), HH, visual agnosia (difficulty recognizing people, prosopagnosia (difficulty naming people based on looks), dyslexia, colour namin and discrimination problems
- Central territory: central post-stroke (thalmic pain), hemianesthesia, sensory impairments (all modalities), contralateral hemiplegia, oculomotor nerve palsy
vertebrobasilar artery syndrome
Vertebral artery supplies the cerebellum and the medulla
-basilar artery supplies the pons, internal ear, and the cerebellum
-can produce both contralateral and ipsilateral S & S
Common characteristics
-Ataxia (ipsilateral), impaired sensation over the face, impaired pain and thermal sensation (contralateral), vertigo, diploplia, dysarthria, dysphagia
locked in syndrome
Syndrome where a patient is aware and awake but has complete paralysis of nearly all voluntary muscles in the body except the eyes and are otherwise cognitively intact
-When the eyes are also paralyzed then it is known as total locked in syndrome
Lacunar syndrome
caused by occlusion of small penetrating arteries supplying the deep brain structures
- Account for more then 20% of all strokes
- Strongly associated with diabetes and hypertension
- lacunar syndrome are consistent with specific anatomical sites
- Pure motor lacunar syndrome
- Pure sensory lacunar syndrome
- othe lacunar syndromes: Dysarthria, clumsy hand syndrome, ataxia hemiparesis, sensory/motor stroke, dystonia/involuntary muscle.
Associated conditions of a stroke
Disorders of speech and language
- Dysphagia
- cognitive dysfunction
- altered emotional status
- hemispheric behavioural differences
- perceptual dysfunction
- seizures
- bladder and bowel dysfunction
- cardiovascular and pulmonary dysfunction
- DVT and pulmonary embolus
- osteoperosis and fracture risk
Hemispheric behavioural differenes
left hemisphere lesion
- Slow, cautious, anxious, and disorganized
- hesitant to try new tasks (require more feedback, support, and encouragement)
- AAware of their deficits
- difficultioes with communicating and processing information, in a sequential linear order
RRight hemisphere lesion
- quick, impulsive, poor judgement
- overestimate abilities, unaware of there abilities
- increased safety risk (Feedback focused on slowing down, and recognizing risks and consequences of actions
- Difficulties with spatial-perceptual tasks and in grasping the whole idea of an activity or task
cerebral shock
Flaccid paralysis and hyporeflexia immediately following stroke
Motor programming for stroke
Apraxia: Motor disorder caused by difficulty planning and performing tasks or purposeful movements (usually left hemisphere damage)
-No primary motor impairments
Ideational apraxia: Inability to produce movement on command or automatically
-No idea how to do the movement (can’t conceptualize or plan
Ideomotor apraxia: Inability to produce purposeful movement of command but is able to perform movement automatically
- Can perform habitual tasks when not asked to do so but cant perform if asked
- Often perservates
Pusher syndrome
Disorder of postural control which may lead to a loss of balance
- Unusual tendency to push weight from the non-hemipareetic (strong side to the hemipareetic (weak ) side with resistance to passive correction
- Posterolateral thalamus involvemtn
Signs of increased ICP
Decreased conciousnes (stupor or coma)
- Altered vital signs
- Widened pulse pressure
- Irregular (cheyne stokes) breathing
- Vommiting
- Headache
- non-reaccting pupils (CN III)
- Papilledema 9optic disc or nerve swelling)
- Progressive impairment of motor function
- Seizure activity
Treatment for elevated ICP
- Elevate head of bed to 30 degrees
- intubate and hyperventilate
- IV mannitol (osmotic agent) promotes fluid removal from CNS while maintaining perfusion
- ventricular drainaage
coma
Arousal system not functioning
- Eyes closed
- Sleep/wake cycles absent
- ventilator dependent
- no auditory, visual, cognitive, or communicative function
- abnormal motor and postural reflexes may be present (Decorticate posturing more common)
Vegetitative state
- Eyes may beopen but awareness is absent\
- brainstem able to manage basic cardiac, respiratory and other functions (weaned offf ventilator)
- Sleeo/wake cycles present
- may startle to visual or auditory stimuli
- meaningful motor, cognitive, or communication absent
- Just react to stimuli but not aware
Minimally concious state
- Minimal evidence of awareness
- cognitively mediated behaviour occur inconsistently
- sleep/wake cycles present
- will localize to noxious stimuli and may inconsistently reach for objects
- may localize to sound location and demonstrate visual fixation and pursuit
Stupor
Almost unresponsive state can be aroused briefly with vigorous repeated stimulation
obtunded
Decreased alertness, sleeps oftern
Glasgow coma scale
3 response scores: eye opening, motor and verbal
scores:
12-15: Mild LOC
9-12: Moderate
3-8 severe
If score is 15 then a more appropriate scale like the ranchos los amigos scale is required
Mild, moderate, and sever TBI
Mild
- GCS: 12-15
- Loss of conciousness: 0-30 minutes
- Altered conciousness: Brief
- Post-traumstic amnesia: 0-24 hours
- Neuroimaging: Normal
Moderate
- GCS: 9-12
- Loss of consciousness: >30 minutes-24 hours
- Altered consciousness: >24 hours
- Post-traumstic amnesia: 24 hours-7days
- Neuroimaging: Normal or abnormal
Severe
- -GCS: 3-8
- Loss of consciousness: >24 hours
- Altered consciousness: >24 hours
- Post-traumstic amnesia: >7 days
- Neuroimaging: Normal or abnormal
special considerations for confused and agitated patients
- Consistency (same place, same time, same person everyday) and create a routine
- Expect no carryoverautomatic skills (procedural memory)
- Model calm behavior
- Expect egocentricity
- Flexibility and option (have back up options in case the original activity doesn’t work, treat pt at appropriate age level, and when appropriate to do so give the patient options
- Safety
Cerebellar dysfunction
Ipsilateral and unilateral motor impairment
- Cerebellum comparees internal feedback with external feedback and generates corrective signals to reduce errors (feedforward mechanism)
- Cerebellar lesions
Midline S&S:
- Truncal ataxia (coordination problem of the trunk muscles)
- Titubation (oscillatory movements of head and trunk
- Orthostatic tremor (shaky leg syndrome)
- Gait imbalance
Hemispheres S&S:
- Limb ataxia
- dysarthria
- hypotonia
Posterior S&S:
- Eye movement disorders (VOR disruption and nystagmus)
- Posture
- Gait imbalance
Cererbellar motor impairments
- Asthenia (generalized muscle weakness)
- Ataxic gait “huggies baby”
- Delayed reaction time
- dysarthria (characterized by scanning speech)
- dysdiadachokineia
- Dysmetria
- Dysnergia
- hypotonia
- motor learning problems
- nystagmus
- rebound phenomenon (ability to stop active movement when resistance is removed)
- Tremor (intention and postural)
cerebellar vs. sensory ataxia
Cerebellar ataxia
- Do dysdiadachokinesia
- dysmetria
- dysynergia
- dysrhytmia
- Will present with ataxic gait
Sensory ataxia
- Do proprioceptive testing
- Will have high stepping or stomping gait
Do romberg test
- If difficulty with eyes open then patient had cerebellar ataxia
- If had difficulty with eyes closed then shows sensory ataxia
Spinal cord injury
Most common MOI
Flexiomn (most commonn in L-spine) Flexion + rotation (Common in C-spine (passenger MVA)) Axial compression hyperextension penetrating injury
Spinal shock
Transient period of areflexia immediately after the injury
- characterized by:
- Absence of all reflex activity (~24 hours)
- Impaired autogenic regulation
- Piloerection (goosebumps)
spinal shock recovery
- Total areflexia (~24 hours)
- Gradual return of reflexes (1 to 3 days
- Uncreasing hyperreflexia - 1 to 4 weeks
- Final hyperreflexia - 1 to 6 months (UMN syndrome)
Tetraplegia
Paraplegia
Loss of motor and or sensory function of all 4 limbs
-Results in lesion of C spine (T1 and above)
Part of thetrunk and lower extremities
-lesion of the T-spine, lumbar spine or cauda equina
Incomplete SCI
Brown-sequard syndrome
- damage to one half of the spinal cord
- Typically due to a penetrating injury
- Will have ipsilateral loss of motor function, (descending lateral corticospinal tract)
- Proprioception, discriminative touch, and vibration sense (ascending dorsal column)
- Contralateral loss of pain and temperature (ascending spinothalmic tract)
Incomplete SCI
anterior cord syndrome
Damage to the anterior cord of the SC
- Typically due to a cervical flexion injury or disruption to vascular supply (anterior spinal artwry
- Loss of motor function, and pain and temperature below the level of the lesion
Incomplete SCI
Central cord syndrome
Most common SCI injury
- due to cervical hyperextension in the cervical region
- compressive forces cause hemorrhage and edema damaging the central portion of the spinal cord
- loss of motor fxn> sensory
- motor loss (UE>LE)
- saccral sensation spared, sacral motor fxn often spared
Incomplete SCI
posterior cord syndrome
- Very rare
- Loss of discriminative touch, proprioception (will see sensory ataxia), and vibration sense
- No motor loss
Primrary complications of an SCI
- Autonomic dysreflexia
- postural hypotension
- Impaired temperature regulation
- blunter HR and cardiovascular response
- Respiratory impairment
- spasticity
- bladder and bowel dysfunction
- sexual dysfunction
Autonomic dysreflexia
Pathological autonomic reflex causing sympathetic overactivity
-Lesions above T6 typically
Order of events:
_Noxious stimulus below level of lesion (Kinked catheter)
-Increased sympathetic outflow (mass reflex response)
-Wide spread vasoconstriction (Increase HR and BP)
-Baroreceptors stimulate leading to increase vagal output causing Decrease HR but insufficient to counteract increase in BP
Interventions:
Sit patient up to decrease BP (lying patient down is contraindicated)
-Check catheter for kink, block, fullness, (notify nurse if needs to be emptied)
NLI C1-C4
-Most severe level of SCI
-paralysis of arms, hands, trunk, and legs (tetrapleegia)
-Patient require assistance with breathing C1-C3, and secretion clearance
-Dependent in all ADLs
-dependent in transfers (mechanical lift)
\
-power wheelchair
-tilt in space or reclining seat
-head, chin, or sip and puff control
NLI C5
Can breathe independently but may be laboured; abdominal binder may improve breathing
- dependent in transfers
- manual wheelchsir with propulsionaids for short distances (flat surfscves)
- Can drive a vsn using adaptive hand controls
- power wheelchsir with adapted joystick for community
NLI C6
- able to perform limited self care activities with tenodesis grasp
- Independent to min assist with sliding board
- independent with manual cough
- wheelchair propulsion possible with use of hand rim projections for short distances
- powerwheelchairfor community
- independent with pressure relief maneuvers in wheelchsir
- can drive car or van with adaptive hand controls
- capable of living independently
NLI C7
Can extewnd elbow allowing for easier use of sliding board transfers
- Can do m ost ADLs by themselves, bed mobility ,such easier
- manual wheelchair with friction surface hand rims and may require assistance with ramos curbs and uneven surfaces
NLI C8
Full use of intrinsic hand muscles aloowing for grasping objects with ease and less needs for adaptive equipment
- Indepent in all ADLs may require adaptive aids
- manual wheelchsir with standard hand rims
NLI T1-T12
The lower the level of the injury in the T-spine the better the trunk control as more paraspinals and abdominals ill be functional
- may use othoses (HKAFO, KAFO) with assistive device for short distances
- wheelchair for community
NLI L1-L3
May use orthoses (HKAFO, HAFO, AFO) with assistive devices for short distances
-wheelchair for community
NLI L4-S1
AFO with assistive device. NLI L4 may choose to use wheelchair for longer distsances
Multiple sclerosis
Chronic inflamatory disease, causing demyelination (oligodendrocytes) in the CNS
- the damaged myelin becomes replaced by plaque (scar tissue)
- sclerotic plaque prevents normal transmission of nerve impulses causing neuro S & S
- believed to be an autoimmune disorder
4 types:
1) Relapse remmiting MS (Most common form)
2) Primrary progressive MS
3) Secondardary progressive MS
4) Progressive relapse-remitting MS
Exacerbated by:
- Relapse (exacerbation) - new and recurrent symptoms that last for at least 24 hours
- Aggravting factors: Viral infection, bacterial infection, disease of major systems, emotional and bodily stress
- Pseudoexacerbation: Transient worsening of MS symptoms. episodes last <24 hours
- Uhthoffs phenomenon - adverse reaction to heat (internal or external)
S & S
- sensory changes (paresthesia or numbness)
- Pain most common is trigeminal neuralgia, paroxysmal limb pain (more common in LE), and headache
- vision changes (opyic neuritis)
- motor dysfunction (central fatigue which is most common and debilitating symptom of MS)
- Speech and swallowing dysfunction
- cognitive and affective changes (Intelect not affected but rather attention and concentration
Exercise has good overall benefit but need to take fatigue and heat into consideration
- Perform exercises in the morning
- exercise in a cool environment
- keep them hydrated
- wear loose, light clothing
- use blow fans
- submax exercise intensities
- take more rest intervals
- dont overwork them
parkinsosn disease
chronic neurodegenerative disorder
-due to loss of dopamine producing neurons in the pars compactia of the substantial nigra of the basal ganglia
4 cardinal signs:
Tremor at rest (pill rolling tremor of the hand)
rigidity (leadpipe and cogwheel) (asymmetrical, proximal to distal)
akinesia (freezing of gait) /bradykinesia (slowness of movement)
postural instability
-kyphosis is the most common postural deformity of PD
Gait: festinating gait
- freezing
- shuffling gait
- decrease arm swing
- decrease trunk rotation
Early S & S:
- Very first sign will be aa loss of smell
- masked face
- Dyphagia
- dysphonia
- micrographia
- festinnating gait
- stooped posture
Later S & S:
- difficulty arising from chair
- difficulty turning over in bed
- cognitive changes/dementia
- sialoorhea (drooling)
- GI dysfunction
- foot dystonia
Intervention programming
- Repetition
- Blocked>random practice
- Decrease cognitive demands
- set up environment to reduce clutter
- use structured instructional sets
- Use external cues
Cues
-Patient with a shuffling gait, cue to take BIG STEPS, pt. step over small styrofoam cups, tell them to imagine taking a big step
Freezing gait: counting, instruct on the count of 3 I want you to take a step, have them step over piece of tape, tap pts leg to cue them to initiate a step
-Decreased gait speed: clap rhythmically or have a metronome for pt to step on the beat
ALS (Amyotrophic lateral sclerosis
chronic degenerative disease of motor neurons in the brain , brainstem, and spinal cord(sensory system is spared)
- Results in UMN snd LMN, the only condition. that presents as both
- Commonly known as Lou Gehrigs disease
Pathophys:
- Progressive degeneration and loss of motor neurons
- UMN in motor cortex and corticospinal tracts
- Brainstem nuclei of. CN V (trigeminal), VII (fascial), IX (glossopharyngeal), X (vagus), and and XII hypoglossal
- LMN in anterior horn of spinal cord
Areas that are spared:
- Sensory system, spinocerebellar tracts
- Brainstem nuclei of CN II (oculomotor), IV (trochlear), VI (abducens) (eye movements are spared which is beneficial for communication
Most common and fatal motor neuron disease in adults (due to respiratory failure causing mortality (3-5 year life expectancy)
Characteristics:
- UMN and LMN syndrome
- Asymmetrical distribution
- Distal> proximal progression
- Caudal>rostral spread within spinal cord
- Weakness is the cardinal sign of ALS
- increased risk of pneumonia
- frontotemporal dementia - cognitive impairments common with bulbar onset ALS
- Anterior horn cells of S2
GBS (Guillian - baree syndrome)
An auto-immune disorder that causes inflamation and demyelination of the cranial nerves and peripheral nerve myelin sheaths
- GBS affects LMN, whereas MS affects LMN
- Acute inflammatory polyneuropathy due to an auto-immune response
- Primarily involves schwann cells causing demyelination of peripheral nerves
- Demyelination causes impulse conduction to be slowed down, become dispersed, or blocked
- Potential axonal damage due to inflammation
- Prgresses from distal to proximal
- But recovers from proximal to distal
- Often occurs after recovering from recent infection or illness
- Most often after an upper respiratory tract infection
3 phases
1) progressive deterioration - demyelination and potential axonal damage (don’t do strength, its pointless)
lasts 1-4 weeks
2)Plateau - disease peaks and there is no further progression
3) Recovery - Axonal regeneration and myelination, progressive recovery usually lasts 6 months - 2 years, complete recovery is common, low mortality rate
S & S:
-ANS dysfunction : high risk of CRPS d/t immobility
-Atrophy
-fatigue (one of most debilitating symptoms
-Hyporeflexia and hypotonia
-Pain : Low back and leg muscles most common
-Paresis: Distal to proximal with LE affected more then UE, may include fascial nerve
-Paresthesia : Glove and stocking pattern
-Repiratory: Possible phrenic nerve involvement
-
primrary functions of the vestibular system
1) Gaze stabilization
2) postural stabilization
3) spatial orientatiuon
