Exam 3 - Neurological disorders + Intro to Medical Aspects

Concussion

TBI that alters brain func.; Temporary effects but includes headaches, problems w concentration, memory, balance, coordination

Traumatic Brain Injury (TBI)

Blow/jolt to/penetrating head injury that disrupts brain func.

Concussion/TBI causes

• Falls

• Unintentional blunt trauma

• Sports injuries

• Motor vehicle accidents

• Assaults

• Military (blast exposure, accidents)

Fatal TBI risk factors

• Men 3x likely to die than women

• Higher for 65 years+

Non-fatal TBI risk factors

• Men have higher TBI hospitalization/ED rates

• Hospitalization rate highest among 65+

• ED rates highest for 0-4years

• Falls leading cause for all but one group

Specific primary injuries

1. Acceleration/deceleration

2. Discrete focal lesions

3. Diffuse axons injury

Acceleration/deceleration

Head accelerates then suddenly decelerates; Whiplash syndrome

Discrete focal lesions

Direct impact site; Countercoup damage

Diffuse axonal injury

No sign of focal lesion; Molecular disruption

Secondary injuries

• Ischemia

• Hypoxia

• Edema

• Hemorrhage

• Brain shift

• Raised intracranial pressure

Neurobehavioral effects

1. Focal deficits

2. Diffuse deficits

Focal deficits

Specific lg deficit; Paralysis

Diffuse deficits

Cog. disorganization

• Attention

• Perception

• Memory

• Learning

• Organization

SLP role in concussions/TBIs

1. Assessment

2. Therapy (improve daily func. + reintegration)

3. Consultation

4. Patient/family education/training

Dementia

Acquired persistent impairment of intellectual function w compromise in at least 3 of:

1. Language

2. Memory

3. Visuospatial skills

4. Emotion

5. Personality

6. Cognition

Dementia statistics

• Hard to determine incidence/prevalence

• Dependent on diagnosis

• Rising rapidly

Medical/neurocog. Assess. of Dementia

• Required experts

• Denial/compensation from patient

• Goals

• Medical eval.

• Neurocog. eval.

Mild cognitive impairment (MCI)

Serious cog. issues than normal aging, not full dementia

MCI diagnosis

• Normal general cog.

• Normal ADLa

• No DX

• Cog area deficits

Alzheimer’s: Risks

• Age

• Low education

• Low SES

• Living alone

• HX of TBI

• Toxins research inconclusive

Alzheimer’s: Early memory impairment

• Forgetfulness

• Word-finding deficits

Alzheimer’s: Sensory memory impairment

Visual memory

Alzheimer’s: Progression

• Difficulty encoding new info

• Short term memory

Alzheimer’s: Later stages

• Long term memory spared

• Lg., reading, writing, pragmatic skills spared until later

Frontotemporal dementia: Risks

• 20-40% inherited

• Men more at risk

Frontotemporal diagnosis

Possible/probable until autopsy

Frontotemporal dementia: Early Cog. Impairment

• Executive funcs.

• Attention

• Variable memory

Pick’s disease

Frontotemporal dementia type; Frontal lobe atrophy w psychiatric symptoms; Memory loss, fluent aphasia, progressive dementia

Primary progressive aphasia (PPA)

Adult onset, degenerative lg. disorder; Affects:

• Lg areas

• Preservation to perform ADLs

PPA symptoms

• Anomia

• Decreased aud. comprehension

• Stuttering

• Declining verbal memory, reading, spelling

Vascular dementia

Multi-infarct; Sudden onset associated with CA, progresses intermittently; Cog. Impairment varies due to lesion site

Vascular dementia: Incidence + Risks

• Small CVAs over time

• 20% of all

• Same risks as for strokes

Neuropathology: Alzheimer’s

• Neurofibrillary tangles

• Amyloid plaques

  • Defective enzymes

  • Abnormal beta-amyloid proteins

Neuropathology

1. Alzheimer’s

2. Degenerative nerve fibers

3. Pyramidal neuron loss

4. Subcortical relationships

5. Multiple infarcts

6. Toxic metabolic encephalopathy

7. Trauma

8. Anoxia

Neuropathology: Subcortical relationships

• Extrapyramidal syndromes (Parkinson’s, Chorea)

• Depression

• White matter diseases (MS, AIDs-related)

SLP role in Alzheimer’s

1. Identify subtle lg disorders

2. Assessment

3. Therapy (improve lg. + swallowing)

4. Consultation

5. Patient/family education/training

Aphasia

• Group of disorders/syndrome

• Affects verbal comm.

• Multimodal

• Caused by brain damage

Occlusion

Opening of an arterial blood vessel occluded, reducing/stopping blood flow to brain

Occlusion categories

1. Thrombosis (blockage)

2. Embolism (blockage that traveled)

Occlusion causes

Arteriosclerosis (arterial walls thickening/hardening, enlarges them)

Embolic

Extraneous material occluded a vessel:

• Embolus breaks away

• Travels via vessels

• Lodges

• Stops/disrupts blood flow

Transient Ischemic Attack (TIA)

Mini stroke (mimics stroke symptoms) but temporary disruptions;

Signs are transient, about 1hr, completed within 24hrs

Hemorrhage Trauma

1. Subdural

2. Subarachnoid

Blood vessel ruptures without trauma

1. Aneurysm

2. Arteriovenous Malformation (AVM)

Aneurysm rupture

Dilated blood vessel; 85% found in internal carotid artery sys.; Congenital; Some never rupture, some have symptoms before rupture

Arteriovenous Malformation (AVM)

Absent capillary network btwn arteries + veins; Twisted/tangled vessels; Congenital

CVA Risks

• Hypertension

• Ateriosclerosis

• Obesity

• Sedentary lifestyle

• High cholesterol

• Family history

• Diabetes

• Stress

• Smoking

CVA Symptoms

• 1sided paralysis

• 1sided sensation loss

• Speech + lg difficulties

• Visual loss, double vision, dizziness

CVA Diagnosis

1. CAT/CT (Computerized Tomography)

2. MRI (Magnetic Resonance Imaging)

3. EEG (Electroencephalogram)

CAT/CT

• (Not very clear) sectional brain x-rays

• Cheap

• Widely available

• No-invasive

• Useful for other abnormalities

MRI

• Not x-rays

• Cheap

• Widely available

• Noninvasive

• Generates strong magnetic field

• Locates certain molecules

• “Slices” of imaging

• Not for people with metal inside body

EEG

• Measures brain’s electrical activity (not struc.)

• Not accurate (only can be used when active seizure, etc.)

CAT/CT: Preferred

• For acute hemorrhage

• When MRI not prohibited

• Asses. struc. not func.

MRI: Preferred

• Infarcts, tumors, blood vessel abnormality

• Asses. struc. not func.

Circle of Willis

3 cerebral arteries

• Originate from circular arterial sys. at brain’s base

• Ant. To brain stem

• Includes small comm. arteries

Circle of Willis: Lower neck

• L/R common carotid arteries

• Become in/external carotid artery on each side of larynx + spinal column

• Internal arteries proceed here

• At brain’s base, Internal carotid artery

Circle of Willis: Lower neck split

Splits in 2 directions:

1. Outward - MCA (Mid. Cerebral artery)

2. Forward - ACA (Ant. Cerebral artery)

Circle of Willis: Up neck

2 Arteries runs post. to carotids

1. L/R vertebral arteries - run up either spine vertebrae

2. Join + become Basilar artery - splits into 2 PCA

Circle of Willis: Ant. Boundary

By ACA; Linked by ant. comm. artery (connects 2 together)

Circle of Willis: Post. Boundary

By division of Basilar artery into PCA

Circle of Willis: Lat. Boundary

United by post comm arteries to internal carotid arteries; Join backside where MCA + ACA are (completing the circle)

An aneurysm in a part of the Circle of Willis may…

Compress the Optic Chiasm + result in visual field loss

Circle of Willis: Anatomy

1. 2 PCAs

2. 1 Ant. Comm. Branch

3. 2 Post. Comm. Branches

4. 2 ACAs

Circle of Willis: Blood Supply

1. Internal carotid

2. Vertebral artery

Circle of Willis Blood Supply: Internal Carotid

1. Ant. Cerebral artery (ACA)

2. Mid. Cerebral artery (MCA)

3. Post. Comm. Artery (PCoA)

Anterior Cerebral artery (ACA)

• Medial surface of brain

• Inferior branch

• Superior branch

Mid. Cerebral artery (MCA)

• Motory + Sensory areas involved in speech, hearing, lg. func.

• Main vessel in Sylvian fissure branches to lateral cortex

• Branches identified as superior + inferior + as frontal, parietal, occipital, or temporal

Post. Comm. Artery (PCoA)

PCA

Vertebral artery

• Basilar artery (bifurcates)

• PCA - medial surface of occipital lobe, base of temporal lobe, primary visual area

Recovery: Acute phase

5 days or 4-6wks post onset

Spontaneous recovery

“Comes back to them”; Hours/wks/mnths immediately following onset; Varies on severity

Sparing of func.

Failure to detect loss of func. due to undamaged brain regions

Recovery

• Restitution of lost func

• Substitution of near means of achieving goal of func/strategies

Acute phase

• Ischemic stroke w/ edema/swelling

• Thromboembolic occlusion likely temporary

• Collateral circulation

• Safety valve alt routes

Determining prognosis

• Dependent on swelling reduction, circulation return to undamaged hemi

• Recanalization + collateral circulation → unstable med condition

• Better determined 1mnth post-onset

Motor speech disorders

1. Apraxia of speech

2. Oral apraxia

3. Limb apraxia

Apraxia of speech (AOS)

Motor programming + planning disorder

• Accompanies Broca’s + Global aphasia

• Damage to area 44 (cause likely CVA)

Apraxia of speech symptoms

• Phon. Subs. (Paper → taper)

• Speech initiation difficulty

• Groping, awkward, labored speech

• Slow rate/short sentences (Leaves out functor words)

Severe AOS symptoms

Verbal apraxia

• Limited speech sounds repertoire/recurrent utter

• Few meaningful utterances

• Unintelligible utterances

• Predictable errors

AOS: Principles

1. Stimulus selection type

2. Simple → complex

3. Self monitoring

4. Feedback

5. Consistent/variable practice

6. Specific Protocols

AOS: Stimulus selection type

• Choose something client can do, then move up

• Meaningful vs. non

AOS: Simple → Complex

Repetition builds pathways to brain; Don’t let them build it the wrong way!

• More instruction

• Cuing hierarchies (“Fade out”)

• Utter length

AOS: Protocols

• Rosenbeck’s 8 step continuum

• MIT

• Phono-motor treatment

Phono-motor treatment

Therapy that “goes back” to baby-like talking, etc; “Babbling” → CVC → etc.; Can be verbal, motor, kinesthetic

Flaccid Dysarthria symptoms

• Breathy, hoarse respiration

• Hypernasal resonance

• Imprecise artic.

• Monopitch/loudness prosody

Flaccid dysarthria clinical traits

• Weakness

• Hypotonia (not a lot of tone)

• Hyporeflexia

• Atrophy

• Fibrillation/fasciculation

Flaccid dysarthria

LMN disorder (CN)

Spastic dysarthria

UMN lesion (Corticobulb tract)

Spastic dysarthria clinical traits

• Hypertonia

• Hyperreflexia

Ataxic dysarthria

Cerebellar lesion (Balance-related); 1/3 related to degenerative diseases

Ataxic dysarthria clinical traits

• Prosody difficulties

• Pitch/loudness changes

• Irr. Artic. Errors

• Irr. DDKs/AMRs/SMRs (can’t keep pattern movement)

Mixed dysarthria

1+ dysarthria types; Spastic + flaccid (tract + CN wiped out)

Mixed dysarthria types

1. ALS

2. MS

3. Shy-drager syndrome

Hyperkinetic dysarthria

Basal ganglia/cerebellum lesion

Hyperkinetic dysarthria clinical traits

• Invol. Movement

• Tics (Tourrette’s)

• Chorea

• Athetosis (Snake-like movement)

• Tremors

Hypokinetic dysarthria

Basal ganglia lesion

Hypokinetic dysarthria clinical traits

• Parkinson’s related

• Resting tremor

• Rigidity

• Monopitch/loudness

• On/off effect

• Can affect swallow

Dysphagia

Swallowing disorder that can socially/emotionally affect one’s life; Anyone w TBIs, strokes, tumors, babies (cleft, neurolo., congenital) can get it

4 Swallowing Phases

1. Oral preparation

2. Oral transfer

3. Pharyngeal

4. Esophageal

Oral preparatory phase

Voluntary yet automatic (bingeing w/o realizing); AKA mastication;

Variable actions/timing based on:

1. Material (crunchy, liquid)

2. Person (teeth/dentition, arousal/how aware)

3. Chewing preference