Neuro board preppers

Frontal lobe

anterior cerebral artery

NO homonymous hemianopsia

broca’s aphasia

parietal lobe

middle cerebral artery

apraxia and anosognosia

occipital lobe

posterior cerebral artery

visual deficit, agnosia, cortical blindness

temporal lobe

middle cerebral artery

hearing and memory

cerebellum

vertebral arteries

lack of coordination

intention tremors

dysdiadochokinesia, dysarthria, and dysmetria

basal ganglia

anterior cerebral artery

bradykinesia

resting tremor

rigidity

thalamus

posterior cerebral artery

thalamic pain syndrome

pushers syndrome

hypothalamus

posterior cerebral artery

altered basic life functions

altered functioning of anterior pituitary gland

brainstem

vertebral arteries

cranial nerve palsy

leads to death

left hemisphere injury

right sided sensory and motor deficits

difficulty with producing language (written and spoken)

slow and cautious

right hemisphere injury

left sided sensory and motor deficits

unable to understand nonverbal communication (body position, facial expression, and social cues)

poor hand eye coordination and kinesthetics

quick and impulsive

CN III

oculomotor

motor

turns eye up, down, in, elevates eyelid, and constricts pupil

CN IV

trochlear

motor

turns the adducted eye down (looking at nose)

CN VI

abducens

motor

turns eye out

CN V

trigeminal

motor and sensory

temporal and masseter muscles

face and cornea sensory

CN VII

facial

motor and sensory

facial expression

taste

CN VIII

vestibulocochlear

sensory

vestibular ocular reflex, cochlear function

CN XI

spinal accessory

motor

trapezius, SCM muscle function

glascow coma scale

mild brain injury: 13-15

mod brain injury: 9-12

severe brain injury (coma): <9

mini-mental status examination (MMSE)

cognitive dysfunction test

max score of 30

severe mental impairment: <= 15

stereognosis

object placed in patients hand and they identify off of touch

graphesthesia

patient is able to identify a letter drawn into their hand

barognosis

pt is able to determine different s weights placed into hand

homonymous hemianopsia

loss of contralateral half of vision field in both eyes

R hemi damage = L field vision loss

agnosia

inability to recognize familiar objects with one sensory modality

apraxia

inability to perform purposeful movements when there is no loss of sensation, strength, coordination, or comprehension.

decorticate rigidity

UMN lesion

flexor in UEs

extensor in LEs

diencephalon lesion

decerebrate rigidity

UMN lesion

extensor in UEs and LEs

brain stem lesion

meningitis

A bacterial or viral infection causing inflammation of the meninges of the spinal cord or brain.

encephalitis

Viral (herpes simplex) or bacterial infection causing severe inflammation of the brain.

brain abscess

encapsulated collection of pus accumulated in the brain that is a localized infection

Amyotrophic lateral sclerosis

UMN (increased reflex, spasticity) and LMN (distal to proximal). Cognition is not affected.

multiple sclerosis

UMN, demyelination of white matter. Series of relapses and remissions.

relapsing remitting

relapses every 3-5 years with no long term deficits. Some recovery is expected.

Primary Progressive

relapses every 1-3 years with long term deficits. “temporary” recovery expected 30+ years

secondary progressive

relapsing remitting progressed into secondary progressive due to illness, stress, pregnancy, or trauma. long term deficits

progressive relapsing

short form of MS, death within 3-7 years. Time between relapses decreases and get worse. Rare form of MS.

anterior cerebral artery syndrome

LE > UE

ataxia

Middle cerebral artery syndrome

UE > LE

homonymous hemianopsia (most common with MCA)

apraxia

only syndrome that produces SIG memory loss

posterior cerebral artery syndrome

visual problems

thalamic pain syndrome

pushers syndrome (twds bad side)

post. = occipital = vision

vertebrobasilar artery syndrome

CN involvement

cerebellar dysfunction

ataxia

wallenburg syndrome

death

internal carotid artery syndrome

death common

s/s of ACA and MCA

Brunnstrums stages of recovery - stage 1

Stage 1 lasts 4-6 weeks presenting with flaccidity and numbness on contralateral side. Joint approx + sensory integration with functional mobility for ADLs and safety.

Brunnstrums stages of recovery - stage 2

Stage 2 lasts 4-6 weeks with spasticity still present (distaly to proximally), synergy patterns movement begins. Contracture prevention (unwinding), functional mobility + safety, and primarily doing PNF.

Brunnstrums stages of recovery - stage 3

Stage 3 lasts 6-12 weeks with spasticity reaching its peak, synergies are our only movement with no movement likely. Still preforming contracture prevention (>48 hrs to form), functional mobility, and working to unwind spasticity (once every <48hrs)

Brunnstrums stages of recovery - stage 4

Stage 4 lasts 4-6 weeks and where isolated joint control begins as synergies and spasticity decline the emergence of isolated joint control. Continuing with contracture prevention, PNF, NDT, motor learning, and functional mobility. Spasticity is declining proximally to distally.

Stage of largest decrease in spasticity.

Brunnstrums stages of recovery - stage 5

Stage 5 lasts a variable amount of time and we now have possible movement out of the synergy patterns. Contractures are no longer a a concern and all techniques available for TX.

Ranchos Los Amigos - Level 1

No response, unconscious, pt is in severe coma.

Ranchos Los Amigos - Level 2

Generalized response but still in mod coma.

Pt responds to noxious stimuli, such as sternal rub, but response is general (opening eyes).

Ranchos Los Amigos - Level 3

Localized response but still in a mild coma.

Pt responds to noxious stimuli, such as a sternum rub, and will acknowledge where pain is felt.

Ranchos Los Amigos - Level 4

confused-agitated requiring 2 people present in room during treatments.

Pt has no memory and is in a state of fear (biting, kicking, screaming). Pts behavior is bizarre and non-purposeful.

Ranchos Los Amigos - Level 5

confused-inappropriate where pt can now attend group therapy.

Pt counts to have no memory but no longer has fear of environment and people. Responds to SIMPLE commands but responses are non-purposeful. Lacks ability to focus attention of specific tasks and reacts/responds on an automatic level.

Ranchos Los Amigos - Level 6

confused-appropriate where pt now has return of old memory.

Pt shows signs of goal directed behavior, new learning still affected so there is no carryover for new tasks.

Ranchos Los Amigos - Level 7

automatic-appropriate where new learning begins.

Pt goes through daily routine automatically robot-like. Carry-over for new learning begins. Judgement counts to remain impaired. Pt requires structure and routines to operate appropriately.

Ranchos Los Amigos - Level 8

purposeful and appropriate

near normal function

ASIA - A

complete, no motor or sensory function below the level of the lesion

ASIA - B

incomplete, sensory but not motor

ASIA - C

incomplete, sensory is normal. motor function. muscle grade less than 3.

ASIA - D

incomplete, sensory normal. Motor function. muscle grade 3 or more

ASIA - E

normal, motor and sensory are both normal

complete cord lesion

UMN lesion with complete B loss of all sensory modalities and B loss of motor function. Spastic paralysis below level of the lesion. There is a loss of bladder and bowel functions w/ flaccid bowel and bladder.

central cord lesion

UMN lesion with B loss of pain and temp, and B loss of motor function primarily in the UEs. Preservation of proprioception and discriminatory sensation. This is a hyper-extension injury in the cervical region with the UEs>LEs.

Brown sequard syndrome

UMN lesion characterized by ipsilateral loss of vibration, pressure, motor function, and proprioception, alongside contralateral loss of pain and temperature sensation, typically resulting from a lateral-cord injury such as a gun shot or stabbing.

anterior cord syndrome

UMN lesion with bilateral loss of motor function, pain, and temperature sensation below the level of the injury, typically caused by hyper-flexion cervical injuries (diving), while preserving proprioception and vibratory sensation within the dorsal columns.

posterior cord syndrome

UMN lesion characterized by bilateral loss of proprioception and discriminative touch, with preservation of motor function, pain, and light touch. This rare condition is typically caused by direct trauma to the spinous process, resulting in the inability to perceive body position in space despite maintained movement and sensation.

Cauda Equina injury

LMN lesion occurring at or below the L2 level. It is characterized by flaccid paralysis, the absence of spinal reflex activity, and neurogenic (flaccid) bladder and bowel dysfunction. Due to the peripheral nature of the nerve roots involved, some degree of recovery is typically expected.

autonomic dysreflexia

Spinal cord injury at or above the T6 level. This is a medical emergency triggered by a noxious stimulus, such as a full bladder, bowel impaction, or tight clothing. Clinical presentation includes paroxysmal hypertension, bradycardia, severe headache, and diaphoresis. Immediate management involves elevating the patient's head, identifying and removing the inciting stimulus, and initiating emergency medical intervention.

wallerian degeneration

The process of axonal and myelin sheath degeneration that occurs in the peripheral nervous system (PNS) distal to the site of an axonal injury.

neuropraxia

A transient nerve conduction block caused by a crush or pinch injury, leading to localized demyelination without axonal disruption; commonly referred to as Saturday night palsy.

axontmesis

A nerve injury involving damage to the axon caused by a severe crush or stretch, where the connective tissue framework remains intact, allowing for potential full recovery through axonal regeneration.

neurotmesis

Severe nerve injury characterized by the complete disruption of both the axon and its surrounding connective tissue sheath, typically resulting from a laceration; this typically leads to a loss of nerve function and often requires surgical intervention for potential recovery.

Guillain-Barre syndrome

A lower motor neuron disorder involving demyelination of the peripheral nervous system (white matter). It typically presents with distal-to-proximal progression, beginning in the feet. The condition follows three clinical phases: the ascending phase (3–4 weeks, requiring limited therapy), the stabilization phase (7–14 days, involving aquatic therapy), and the descending phase, which marks the onset of recovery and the initiation of standard rehabilitation.

myasthenia gravis

lower motor neuron disorder characterized by cranial nerve involvement, typically beginning with the eyelids (CN III), progressing to facial muscles (CN VII), then the throat and pharynx (CN IX and XII), and potentially impacting respiratory function via the phrenic nerve. The progression follows a cranial-to-caudal or proximal-to-distal pattern.

bells palsy

lower motor neuron disorder involving the facial nerve (CN VII), characterized by unilateral facial drooping, an acute onset lasting 3–4 weeks, preserved sensation, and a high likelihood of full recovery.

trigeminal neuralgia

Trigeminal neuralgia (CN V), also known as "tic douloureux," is a debilitating condition characterized by sharp, stabbing, shooting, or burning facial pain. It is frequently associated with multiple sclerosis and facial shingles.

Complex regional pain syndrome

abnormal response of the PNS typically following nerve trauma or localized injury. It progresses through three stages: Stage 1 involves increasing pain and dysfunction; Stage 2 sees worsening pain, skin changes, and the onset of joint dysfunction; and Stage 3 involves persistent pain that may plateau as other symptoms begin to recede. The condition generally lasts 12–18 months.