811 Neuro Exam 2

what is the difference b/t a primary brain tumor and secondary brain tumor

-primary: originates in CNS
-2ndary: metastatic tumor originating elsewhere in body & spreading to brain

what CA's most frequently result in metastases to the brain

lung, breast, GI's, kidney, melanoma

What arise from glia cells/supportive tissues?

-Frequently located in cerebral hemispheres (adults) & cerebellum (children)

-Astrocytomas, Oligodendrogliomas, ependymomas

glioma

the staging/grading of gliomas are divided into 4 grades:

grade IV = glioblastoma → most severe, aggressive, & highly malignant (grows rapidly & invades nearby tissues)
poor med prognosis if stage 4 → <40% will survive 1 yr; <5.5% have a 5 yr survival rate (< 5.5% of pt will reach 5 yr mark)

What are derived from astrocytes & glia cells?

-most common glial tumor in both adults & children

-frontal lobe (adults) cerebellum (children)

astrocytoma

What are slow growing, progressive tumors?

-generally found in cerebral hemispheres

-better prognosis than other gliomas

Oligodendroglioma

What brain tumors arise from ependymal cells (that line ventricles)

-usually occur in ventricles & surrounding tissue (ventricles make & distribute CSF)

-most commonly occur in 4th ventricle

ependymoma

What brain tumors are always malignant embryonal tumors → always grade IV tumors?

-Frequently found in cerebellum

-Commonly grow into 4th ventricle, causing CSF to get stuck in 4th ventricle → leads to ↑ ICP

-75% occur in children

medullablastoma

What brain tumors are slow growing (allows for more time to find & treat tumor)

-Originate in dura mater or arachnoid membrane

-Generally benign

meningiomas

What are benign epithelial tumors that are low growing?

-In pituitary gland → impact hormone secretions (hormones affected will determine presentation)

pituitary adenomas

What are brain tumors composed of neoplastic Schwann cells (myelin production in PNS)

-Arise on cranial nerves or spinal nerves. Acoustic neuroma indicates CN VIII affected via this schwannoma

schwannomas

What tumors arise from cells in lymphatic system? Rare

-5 year survival rate = 33% → poor prognosis

primary CNS lymphomas

what are common signs and symptoms seen in frontal lobe tumors?

-hemiparesis
-seizures
-gait disturbances
-cognitive impairments (↓ executive function, disinhibition, ↓ lack of initiation, poor insight/judgment)

what are common s/s seen in parietal lobe tumors?

-contralateral sensory loss & hemiparesis
-impaired speech
-agnosias: difficulty recognizing objects, people, sounds
-apraxias: difficulty connecting motor plan to executing a mvmts→ ideational (unable to execute motor tasks/can not think of idea) vs ideomotor (can come up w/ plan but can not execute it)
-visual spatial disorders

what are common s/s seen in occipital lobe tumors?

-visual loss/blindess
-hallucinations

what are common s/s seen in temporal lobe tumors?

-auditory or perceptual deficits
-impaired memory, learning
-emotional dysregulation

what are common s/s seen in cerebellar tumors?

-ataxia
-nystagmus
-dizziness

what are common s/s seen in brainstem tumors? (pons, midbrain, medulla)

-gait disturbances
-focal weakness
-diplopia
-facial numbness
-HA
-vomiting
-personality changes
-syncope
-hypo-or hyperventilation
-orthostatic hypotension
-apnea

what are common s/s seen in pituitary tumors?

sxs dependent upon hormone(s) impacted

what is a brain abscess caused by

Microorganisms reach brain thru penetrating wound, local infection, or distant site of infection

what is the classic triad of a brain abscess

-Increased ICP
-Focal neuro deficit
-Fever

What is a bacterial or viral infection of CNS spread thru CSF (spreads via CSF causing inflammation) w/ an accompanying inflammatory process affecting pia & arachnoid mater, subarachnoid space, & superficial adjacent tissues of brain & spinal cord

meningitis

what is the etiology of bacterial meningitis (order of events)

-bacterial agent enters CSF & causes inflammation in brain leading to obstruction of ventricles → CSF accumulates in ventricles leading to ↑ ICP & ↓ cerebral BF, causing systemic BP to ↑ because it is compensating for ↓ BF
(bacteria → inflammation → obstruction of ventricles → accumulation of CSF → ↑ICP → ↓cerebral BF → ↑ systemic BP)

what are the clinical signs of bacterial meningitis?

-fever (infection)
-HA (due to ↑ ICP)
-vomiting (medullary center stimulated)
-papilledema (↑ ICP can swell optic nn.)
-altered consciousness
-convulsions
-nuchal rigidity (irritation to subarachnoid space)→ painful cervical flexion

what are the 3 clinical tests that can help identify bacterial meningitis?

-Kernig's Sign: Pt in supine, bring pt hips to 90° flexion & then attempt to extend knee → resistance felt = (+) & can be present in bacterial meningitis BUT could also occur due to HS tightness or sciatic nerve tension
-Brudzinski sign: Pt in supine, PT brings pt into cervical flexion & observes either knee or hip flexion = (+)
-Jolt Sign: Turn pt's head quickly → (+) = worsens pts HA

what is the etiology, sxs, & mgmt of aseptic meningitis

-Etiology: contamination of CSF w/ a viral agent
-S/S: similar to bacterial meningitis BUT less severe
-Medical Mgmt: sx mgmt→ clinical course is shorter & benign; NOT a medical emergency

what is the etiology of brain encephalitis

-Inflammation of parenchyma (fnx tissue of our organs/where mitochondria lives) & surrounding meninges
-Inflammation can be caused by many agents → often viral invasion of cells of brain or SC (Virus in brain or SC)

what are the sxs associated w/ brain encephalitis?

↑ temperature
-HA
-Nuchal rigidity
-Vomiting
-Malaise
↑ ICP can lead to hemiparesis, LOS, CNS palsy, ataxia

What is a condition where primary pathophysiological processes are alternation in FUNCTIONING of brain networks rather than abnormalities in brain structures?

Communication b/t 1 side of brain to other side is impaired

Seen w/ fMRI → whole brain will light up

-includes motor &/or sensory sxs that are genuinely exp

-Often will overlap w/ a neurologic disorder

functional neurologic disorder (FND)

what are 5 types of FND

-Functional Movement Disorder (FMD)
-Complex Regional Pain Syndrome
-Functional Seizures
-Functional Cognitive Disorders
-Persistent Postural Perceptual Dizziness (PPPD)

What is involuntary, learned habitual mvmt pattern driven by abnormal self-directed attention?

-Complex combinations of physical, psychological, & social influences on brain fnx contribute to disorder

-Limbic system firing as motor = hard to differentiate them

-Often triggered by a physical, psychophysiological, or emotional life event

functional movement disorder (FMD)

what are the common symptoms of FMD?

-tremor
-Gait Disorder
-Dystonia
-Weakness/paralysis

What are the 6 aspects contributing to the pathophysiology of FMD?

-physical limitations: prior trauma, concussion/WAD, pain
-autonomic: low HRV, ↑ resting HR/cortisol/arousal
-lifestyle: impaired sleep, stress/fatigue, low self-efficacy
-motor control: impaired set shift & adaption, impaired motor inhibition, abnormal activation of SMA, ↓ feedforward signaling, ↑ activity in cingulate
-sensory: abnormal sensory processing, sensory avoid, low registration, ↓ sensory attenuation, ↑ mirror neuron activation
-psychosocial: adverse childhood events, anxiety/depression, impaired emotional processing/attention/self-agency, amygalda hyper-activation

What are common FMD triggers w/in each of the 6 aspects contributing to the pathophysiology of FMD?

-physical limitations: injury, nerve tension, muscle tightness/soreness, pain
-autonomic: fear, lowered HRV, exercise/exertion, change in position, change in BP or HR
-lifestyle: impaired sleep, change in diet, poor pacing, change in routine
-motor control: attention brought to body or sxs, change in environment or surface while walking, transitions, abnormal mvmts in others
-sensory: change in sensory stimuli or too much/too little stimuli
-psychosocial: adverse childhood event/trauma, anxiety/depression, lack of control or autonomy

What are important FMD assessment focuses w/in the 6 aspects that contribute to FMD?

-physical limitations: neural dynamics, joint mobility, strength
-autonomic: breathing pattern, response to breathing, active stand test
-lifestyle: sleep hygiene index, diet & eating schedule, perceived stress scale
-motor control: change w/ transitions, response to mirror/imagery feedback, use of OPTIMAL
-sensory: joint position & body awareness, change in sensory exp & weighting, vestibular exam
-psychosocial: HADS, PCS, PHQ-9, self efficacy scale

What are important FMD tx options withiw/in n the 6 aspects that contribute to FMD?

-physical limitations: nerve/ST mobs, flexibility, strengthening
-autonomic: HRV biofeedback, breathwork, grounding, graded exercise training
-lifestyle: diet, sleep hygiene, stress mgmt, ADL training
-motor control: OPTIMAL, graded exposure, demo mvmt capabilities
-sensory: higher order sensory training, graded exposure, vibrations/TENS
-psychosocial: listening, reflection/validation, education

What is an acute inflammatory demyelinating polyneuropathy (AIDP) → nerves are degenerated (↓ info conduction speed) leading to polyneuropathy?

-Immune-mediated disease process that attacks nerve roots & peripheral nerves (PNS) = LMN sxs

Guillian barre syndrome

what findings lead to a medical diagnosis of guillian barre syndrome?

-elevation of proteins in CSF
-slowed velocity/amplitude on nerve conduction test
-absence of fever at onset of symptoms

what will more than ⅔ of pt's w/ GBS have 2 wks before the start of their sxs?

some precipitating infection (GI bug, respiratory illness, flu shot) 2 wks before sxs start

what are 7 hallmark sxs of GBS

-severe midline back pain &/or sensory changes
-progressive muscle weakness over a 10-12 day period that starts from toes & moves up (distal → proximal)
-diminished or absent reflexes (LMN)
-ANS signs
-respiratory signs
-facial muscle impairments due to facial nerve involvement (50%)
-pain & fatigue

what is the long standing impairment commonly seen in pt's w/ GBS?

↓ strength of anterior tibialis**
↓ strength of hand/feet intrinsics
↓ strength in glutes and quads

What is inflammation of SC that occurs in a focal location across 1 spinal segment? (messages unable to pass inflamed segment)

-Causes injury to myelin sheath around nerves → leading to sensory, motor, & autonomic dysfunction in that area

transverse myelitis (TM)

what type of sxs will be seen in transverse myelitis (TM)

-UMN sxs
-sensory, motor, & autonomic signs below level of injury

What is new weakening of muscles previously affected by polio OR weakness in muscles not originally thought to be affected by polio?

-Degeneration of nerve terminals in the motor unit

post-polio syndrome (PPS)

what sxs are seen in post-polio syndrome (5)

-Slow progressive muscle weakness
-Asymmetrical or "patchy" presentation
-Abnormal fatigue
-Muscle atrophy
-Joint/muscle pain/tenderness
-LMN

What are rapid localizations stimulated by images from periphery? (detection of motion or change in light intensity)

-Can be horizontal or vertical

saccades

What is it when 1 eye turns inward towards nose during divergence?

esotropia strabismus

What is it when 1 eye turns outward during convergence?

exotropia strabismus

What is loss of incoming sensory info from ½ of visual environment contralateral to side of lesion? (ex. L hemiplegia/field cut due to R CVA)

visual field cut/homonymous hemianopsia

What is total failure to appreciate incoming info due to occipital lobe damage?

-cannot process visual info

cortical blindness

What is lack of awareness or ↓ awareness of sensory stimulation on contralesional side of body OR space/environment?

-Often unaware of deficit & indifferent to that side of body

-Can occur if vision is intact or impaired

-R hemisphere lesion > L hemisphere lesions

-Often occurs w/ posterior parietal or thalamic lesions

unilateral spatial inattention/neglect

what is failure/decreased ability to move contralaterally to damaged hemisphere?

-typically seen in eyes, head, limbs, or trunk

-Not deficit of motor pathway but failure to move in contralateral space to damaged hemisphere

action-intentional disorder (motor neglect)

what is lack of or decreased awareness of sensory stimulation in contralesional hemispace?

inattention (sensory neglect)

which inattention is most common/which brain lesion side is most commonly seen w/ inattention?

-L inattention most common because R hemisphere is responsible for both R & L
-L hemisphere attends to only R hemisphere which is why it is less common
-L inattention > R inattention (R hemisphere lesion > L hemisphere lesion)

What is lack of awareness or denial of a paretic extremity? (do not recognize it is theirs)

-Lack of insight concerning paralysis/disability

-often resolves spontaneously in 1st 3 months

anosognosia

What is impairment in body scheme → lack of awareness of structure of body & relationship of body parts to oneself or to others?

-Difficulty w/ activities related to following instruction for mvmt during transfers, dressing, exercise

-Lesions often in parietal lobe

Exam: point to body parts on self or PT, imitate PT mvmt, answer questions related to relationships of body parts (no R/L)

somatognosia/body agnosia

What is inability to identify the L & R sides of one's body or body of examiner?

-Lesions often in parietal lobe

Exam: ask pt to point to their body parts using R/L

right/left discrimination

What is inability to visually distinguish a figure from its embedded background?

-Difficulty determining end of stair on descent/edge of step

-Lesions often in parieto-occipital region

figure/ground discrimination

What is difficulty understanding/remembering relationship b/t locations? (difficulty w/ route findings)

-Lesions often in parietal cortex

topographical disorientation

What is an inaccurate judgment of direction, distance, & depth?

-Lesions often in posterior R hemisphere

depth/distance perception

What is inability to recognize familiar objects despite normal vision?

-Cannot visually identify an object, but can identify once using another sense

-Lesions often in the occipito-temporal cortex

visual agnosia

What is breakdown b/t concept (idea of mvmt) & performance? (execution of mvmt)

-Cannot perform task on command BUT can perform spontaneously

-Lesions often in frontal or posterior parietal lobes

-Ex. ball is rolled to the pt & they kick it. Ball is rolled to the pt & you ask them to kick it but they are unable to when you ask them to kick it

ideomotor apraxia

What is failure to conceptualize a task? (unable to figure out idea of mvmt & can not do actively w/ command or w/o one)

-Cannot perform task automatically OR on command

-Lesions often in parietal lobe

-Ex. Unable to kick ball spontaneously (w/o command) as well as w/ command = ideational

ideational apraxia

What is a brief assessment for cognitive ability overtime? Assesses 11 items in 7 categories (orientation to time & place, registration of 3 words, recall of 3 words)

<24/30 suggest cognitive impairment

Mild = 18-24

Severe = 0-17

mini-mental status examination (MMSE)

What is a brief assessment of cognitive ability for mild cognitive impairment that assesses 16 items in 11 categories? (naming, attention, language, abstraction, orientation)

Highest score = 30 (cut offs vary by dx)

Normal >/= 26

montreal cogntive assessment (MOCA)

What is the ability to select & attend to a specific stimulus while simultaneously suppressing extraneous stimuli?

attention

What is the capacity to attend to relevant info during an activity?

-pt can maintain attention for a set period of time

-if impaired, pt will drift off while doing a task (such as watching TV)

sustained attention

What is capacity to attend to a task despite environmental visual or auditory stimuli?

-Still able to maintain focus when a train goes by in class

-if impaired, pt may need to stop their activity to response/answer you

focused (selective) attention

What is capacity to move flexibly b/t tasks & respond appropriately to demands of each task?

-Following a recipe while cooking

alternating attention

What is the capacity to respond simultaneously to 2 or more tasks or stimuli when all stimuli are relevant?

divided attention

What are the 2 types of long term memories?

-explicit (declarative) memory: memory for words, scenes, faces, stories, facts; associated w/ explicit learning → conscious verbalization of knowledge of facts & events
-implicit (procedural) memory: unconscious memory, often procedural or "how to"; associated w/ implicit learning → abstract knowledge related to skill learning, habit formation, changes in performance related to experience; how to go about something/do something

what are the 4 components of executive function

-volition
-planning
-purposive action
-effective performance

What is the capacity to determine what needs & wants to do?

-ability to plan for a goal, initiate a task, be aware of environment, & have social awareness

volition

What is identification & organization of steps & elements needed to carry out an intention or achieve a goal?

-ability to weight alternative options & make choices

planning

What is the ability to initiate, maintain, switch & stop complex action sequences in an orderly manner to reach a goal?

purposive action

What is the capacity for quality control → self-monitor & self-correct behavior?

effective performance

What is an acquired communication disorder that is manifested in individuals who were previously capable of using language appropriately?

-often due to focal lesion from stroke or TBI

aphasia

What is not a type of aphasia, but a measure of severity?

-Significant dysfunction in both receptive & expressive language due to significant damage in L hemisphere

-Marked dysfunction across all language modalities

-Damage is usually extensive throughout L hemisphere & is sometimes bilateral

-Has worst prognosis

global aphasia

What is impaired auditory comprehension & fluent speech marked by word substitutions? (difficulty w/ comprehension but able to express themselves)

-due to lesions in posterior portion of the 1st temporal gyrus of L hemisphere (more common after TBI)

-faster rate of speech than normal, may make up words, have numerous errors, use jargon/word salad

fluent/Wernicke's/receptive aphasia

what are communicative strategies for fluent/Wernicke's/receptive aphasia?

-quiet, non-distracting environment
-short, simple instructions
-facilitate communication w/ gestures, demo, slow down rate of speech (a bit)
-written cues

What is comprehension/understanding is relatively preserved, but significant difficulty in verbalizing language? (difficulty w/ expression)

-lesions in anterior aspect of 3rd frontal convolution of L hemisphere (common in stroke)

-limited vocabulary → sometimes unable to talk at all, slow hesitant speech, awkward articulation & restricted use of grammar

non-fluent/Broca's/expressive aphasia

what are communicative strategies for non-fluent/Broca's/expressive aphasia?

-utilize yes/no questions (via cards/comm board) → ask in more than 1 way to determine yes/no bias (ask questions you know the answer to)
-cue individual to point or gesture
-try writing
-try to establish context

What is an impairment of speech production resulting from damage to CNS or PNS that causes weakness, paralysis, or incoordination of motor-speech system?

-can co-exist w/ aphasia

-can impact any component of motor-speech system (respiration/breath support, phonation/speech sounds, articulation/clarity, resonance/transfer of sounds, & prosody/rhythm & pitch )

dysarthria

what are communicative strategies for dysarthria?

-quiet, closed environment
-encourage individual to speak loudly
-cues to slow down as needed
-DON'T ask individual to repeat same thing over & over → clarify what you think they said instead
-DON'T talk for the individual

what is ​​articulatory difficulty in absence of impaired strength or coordination of motor-speech system?

-brain has trouble programming sequence of muscle speech production

-seen in individuals w/ non-fluent aphasia (Broca’s/expressive)

apraxia

what is the clinical presentation of apraxia

-difficulty initiating speech
-articulatory struggling w/ speech sound errors
-periods of error-free speech production w/ ↑ # of sound production errors as utterance length ↑
-slow rate of speech & slow transitions b/t sounds, syllables & words
-impaired prosody

What is a condition that leads to interruption of either eating fnx or maintenance of nutrition & hydration?

-not a cognitive or communication impairment but is common

-often occurs w/ dysarthria

-combo of weakness & poor coordination of muscles required during oral or pharyngeal phases of swallowing

25-50% of individuals post CVA will experience this

dysphagia

what are examples of reversible dementia which has a condition that simulates sxs but is able to be treated?

-alcohol or drug abuse/dependence
-hypoxia
-renal or hepatic failure
-UTI
-stroke, head trauma, brain lesion, seizure
-pharma (benzodiazepines, neuroleptics, steroids, narcotics)
-acute or chronic pain
-sensory deprivation or overstimulation
-constipation or impaction

what are examples of irreversible dementia which is progressive (8)

-AD
-PD
-Huntington's disease
-AIDS
-multi-infarct dementia
-normal pressure hydrocephalus
-alcoholic dementia

What is accumulation of CSF in brain causing ventricles to enlarge but little to no ↑ in ICP?

-Often misdiagnosed as AD or PD*

-Clinical Presentation: Shuffling gait, Changes in mental status, Urinary incontinence

-Tx: ventriculoperitoneal shunt placement in brain to drain fluid

normal pressure hydrocephalus (NPH)

What is the leading causing of dementia? (6th leading cause of death in US)

-d/o caused by nerve cell damage & death in brain due to neurofibrillary tangles & beta-amyloid plaques

-true confirmation = autopsy/biopsy

alzheimer's disease

What stage of AD lasts 2-4 yrs & involves loss of functional skills or orientation, memory loss & lack of spontaneity?

-May need to give up a job or hobby, depression is common

-May lose ability to handle a personal budget, drive, or tell time

-May need to think about whether individual can live alone safely

stage 1 of AD

What stage of AD has progressive memory loss & presence of a variety of neuro sxs?

-Other common sxs include paranoid delusions, hallucinations, agitation, violent behaviors, uncontrollable screaming, apraxia, wandering, repetitive mvmts, change in appetite, WBOS gait

stage 2 of AD

What stage of AD has development of vegetative sxs?

-May become mute, stop eating, become incontinent

-Muscle twitches, spasms of diaphragm, & inability to walk are common

-Emotional responsiveness may be completely absent or only present at a primitive level

-Leads to death

stage 3 of AD

What provides sense/feedback of position in space in relation to gravity?

-Slowest, but "final decision maker" in maintenance of balance → responsible for resolving sensory conflict b/t visual & somatosensory systems

-Drives appropriate motor output (to keep us upright/on feet/balanced) via vestibulocochlear reflex & vestibulospinal reflex

vestibular system

What provides gaze stability of an image/object during head mvmts by generating rapid compensatory eye mvmts in OPPOSITE direction of head mvmt/turn?

-turn head to L, L ocular muscles of both eyes = inhibited, R ocular muscles of both eyes = excited

vestibulocochlear reflex (VOR)

What provides postural stability by generating compensatory body/trunk mvmts to maintain head upright?

vestibulospinal reflex (VSR)

where is the membranous vestibular labyrinth of peripheral vestibular system located & what is contained w/in it?

-location: petrous portion of each temporal bone (base of skull b/t sphenoid & occipital bone)
-each labyrinth contains 5 neural structures that detect head acceleration (3 SCC, 2 otolith organs)

What are the positions/fnx of horizontal SCC, posterior (inferior) SCC, anterior (superior) SCC in each labyrinth?

-positioned at R angles to another allowing for formation of 3 coplanar pairs existing b/t L & R SCC
-rate sensors that respond to angular acceleration (head velocity/how quickly head is moving during rotation) best in their own plane w/ coplanar pairs exhibiting a push-pull dynamic

What are the components of each SCC & their functions?

-SCC are filled w/ ENDOLYMPH moving freely w/in each canal in response to direction of angular head position
-SCC's enlarge at 1 end to form AMPULLA
-w/in ampulla is CUPULA which is a gelatinous barrier that contains sensory hair cells (CILIA = stereocilia (short) & kinocilia)
-mvmt of cilia leads to changes in membrane potential