Neurological Disorders

TBI

craniocerebral trauma

common causes: motor vehicle, accidents, falls, sports

TBI types

• penetrating

• non-penetrating

Penetrating TBI

Open head injury

• foreign object breaks through skull, punctures meninges and enters the brain, pushes bone fragments into brain below fracture

• Impairments often focal (localised) rather than diffuse

Non-penetrating

Closed head injury

• damaged brain without open wound/penetration of foreign substance into brain

• skull may be fractured but meninges intact

• produces more complex symptoms than penetrating - widespread damage

Types of nonpenetrating TBI

• Type 1: Nonaccelerating lesion

• Type 2: Acceleration - Deceleration

Nonaccelerating lesion

• restrained head hit by moving object

• generally less severe consequences

Nonpenetrating TBI

AKA Coup-Contrecoup

• head set into motion by physical forces

• affecting entire tissue - front and back of brain - strains - stressing/straining on white matter fibres

TBI secondary effects

• intracranial hematoma (collection of blood between brain and skull)

• increased intracranial pressure

• seizures

• infections - penetrating TBI is higher-risk

TBI neurobehavioural effects

• Altered consciousness

• impaired reasoning, planning and thinking skills

• memory problems

• confusion & disorientation

• dysphagia

• communication disorders

  • dysarthria, confused language, anomia, problems maintaining topic, impaired social interaction, lack of narrative cohesion

Altered consciousness

• coma - unconscious and unresponsive to most or all external stimuli

• Stupor - generally unresponsive, but pain or other strong stimulus may arouse patient for brief period

• assess using glasgow coma scale

Lacunar infarcts

• type of ischemic stroke

• obstructions of blood flow in smaller deep arteries within the brain

• occur most often in basal ganglia, internal capsule, thalamus and brainstem

• signs develop slowly

Lacunae

small cavities that remain after necrotic tissue is cleared away

Transient Ischemic Attack (TIA)

= ministrokes

• temporary disruptions of cerebral circulation accompanied by symptoms

• symptoms resolve completely within a few mins to 24 hours

• increased risk of stroke with permanent neurological deficit within 5 years

• warning sign of potential strokes to come

CVA ischemia treatment

• thromboembolic processes

  • anticoagulant drugs - reduce stroke by prevention of embolism

  • platelet inhibiting drugs - can reduce risk of recurrent TIAs

• thromboembolytic activating agents (t-PA) = clot-busting drugs

  • restores blood flow by dissolving clot

• carotid endartectomy

  • surgery removing plaque inside carotid artery

• angioplasty/stenting

  • mechanically widening narrowed/obstructed artery

• clot retrieval

CVA recovery

some degree of spontaneous behavioural recovery occurs during period after stroke - whether or not they have rehab

result of

• diaschisis - temporary suspension of fxns of uninjured areas with rich connections with injured brain areas

• reduced blood flow

• edema - swelling due to extra fluid

Brain tumours

• any cell type in nervous can become neoplastic (neoplasia = uncontrolled, abnormal growth of cells)

• nervous system tumours rarely metastize outside CNS

• systemic cancer can matastize to CNS

Types of brain tumours

• neurocytomas = neuronal neoplasms (rare)

• astrocytomas- most common primary CNS tumor = neoplasm from astrocytes - glioma (from glia cells - non-neuronal)

• meningiomas - from meninges

• schwannomas - from Schwann cells

Speech and language problems following neurological disorders

• apraxia

• dysarthria

• aphasia

Apraxia/dyspraxia

dysfunction of motor planning in absence of muscular weakness or muscular dyfunction

• muscles themselves are fine

Types of apraxia

• ideomotor

• oral

• apraxia of speech

Ideomotor apraxia

• impaired ability to carry out skillful purposeful movement in response to a verbal command

• often accompanies aphasia & may be mistakenly identified as comprehension difficulty

Oral apraxia

inability to voluntarily perform nonspeech movements with laryngeal, tongue and facial muscles, in the absence of muscle weakness

Apraxia of speech

• impaired ability to execute voluntarily appropriate movements for articulation in absence of muscular weakness or dysfunction

• inconsistent initiation & sequencing of articulatory speech movements

• often associated with Broca’s aphasia

Dysarthria

• group of speech production disorders caused by oral-motor weakness, paralysis or incoordination

• congenital or acquired

• Not necessarily a language disorder

  • A disorder of motor function

Types of dysarthria

• spastic

• flaccid

• hypokinetic

• hyperkinetic

• ataxic

Spastic dysarthria

• associated with UMN lesions

• usually bilateral lesions

speech characteristics:

• imprecise consonant production

• low pitch

• slow speaking rate

• harsh voice with strained-strangled quality

Flaccid dysarthria

LMN or motor unit lesions

Speech characteristics depend on part of motor unit & specific CN affected:

• imprecise articulation

• hypernasality

• tongue fasciculations

• voice difficulties

Hypokinetic dysarthria

Basal ganglia lesions - associated with PD

speech characteristics:

• monoloudness

• monopitch

• decreased loudness

• breathy voice

• short rushes of speech

Hyperkinetic dysarthria

Basal ganglia lesions - associated with HD

speech characteristics:

• excessive variation in loudness

• variable rate

• irregular articulatory breakdowns

• involuntary movements of oral musculature

Ataxic dysarthria

cerebellar lesions

• caused by damage to cerebellum & its pathways - loss of coordination

• e.g., degenerative diseases, stroke, trauma, tumours, alcohol intoxity

speech characteristics may include:

• excess & equal stress (scanning speech)

• irregular articulatory breakdown

• slow rate & prosodic changes

• harsh voice quality

• excessive loudness variation

Aphasia

• acquired communication disorder caused by brain damage - stroke most common cause

• characterised by impairment of language modalities: speaking, listening, reading and writing

• not result of sensory, motor, general intellectual deficits, confusion or psychiatric disorder

• Types: Broca’s, Wernicke’s, global

Broca’s aphasia

= expressive aphasia

• lesion may be in Broca’s area

• verbal expression

  • Nonfluent & effortful speech

  • Anomia – word finding & recalll

  • Poor/absent grammar

  • Aware of their speaking difficulties

• auditory comprehension

  • usually impaired but comprehend spoken language better than they speak

  • may have difficulties understanding more grammatically complex sentences

Wernicke’s aphasia

= receptive/jargon aphasia

• lesion often in Wernicke’s area

• frequently no muscle weakness - typical site of lesion away from precentral gyrus

• Auditory & reading comprehension

  • severe impairment

• Verbal expression

  • fluent speech with abnormal content

  • often neologisms (made up words)

  • if severe – may be jargon

• Not aware of their difficulties

Other disorders affecting communication

Memory problems

Sensory memory

• 1 st step in information processing

• extremely brief (ms – 2 sec)

• Responsible for holding sensory information for a very short duration after the stimulus has ended

• Acts as a buffer system that allows the brain to register and process incoming sensory input before:

  • Decays

  • Transferred to short-term memory for processing

  • e.g., visual & auditory information storage

Working memory

= active memory

• Storage and manipulation

• limited capacity (~4-7 items)

• Active & conscious

• info must be continually acted upon

  • if not rehearsed memory will decay quickly

• prefrontal & frontal-parietal cortex involved

Short-term memory vs working memory

Short-term:

• static storage with minimal processing—remembering a new telephone number

Broader working memory:

• dynamic and more relevant for understanding higher cognitive functions—doing mental maths

Long-term memory

• relatively permanent storage of info

• 2 main types

  • declarative (explicit) memory

  • nondeclarative (implicit) memory

Long-term Explicit Declarative Memory

Factual info that can be declared

• semantic memory

  • conceptual knowledge--facts, ideas, and concepts

  • e.g. ‘Madrid is the capital of Spain’

• episodic memory

  • info about temporally dated episodes & events

  • e.g. Your first day of Uni, what you had for breakfast, specific and general events

Structures involved in Long-term Explicit Declarative Memory

• medial temporal lobes, incl. hippocampus & surrounding structures

• amygdala, role in emotions accompanying processing of certain memories

Long-term Implicit Nondeclarative memory

Procedural memory (implicit and unconscious)

• broad term for several kinds of memory

  • e.g., motor skills, reflexes, emotional, unconscious

• strengthened by repetition & practice (habit/rote)

  • tying shoelaces, riding a bike, multiplication tables

Structures involved in Long-term Implicit Nondeclarative memory

• motor skills: caudate nucleus, putamen, motor cortex, cerebellum

• emotional implicit memories: amygdala

• conditioned reflexes: cerebellum

Memory disorders

• amnesia

• retrograde amnesia

• anterograde amnesia

Amnesia

• loss of long-term memory

• often refers to declarative memory loss

Retrograde amnesia

loss of memories for events that occurred prior to the trauma or disease causing the memory loss (trouble accessing old memories prior to injury)

Anterograde amnesia

involves loss of memory for events following the trauma or disease (trouble making new memories)

Neuroplasticity

The ability of the nervous system to respond to intrinsic and extrinsic stimuli by reorganising its structure, function and connections

Ability to make new connections, change the way the brain functions and adjust things on the fly

Neuroplasticity can occur

• during development

• in response to environment

• in support of learning

• in response to disease

• in response to therapy

Use it or lose it neuroplasticity principle

Failure to drive specific brain functions can lead to functional degradation

Use it and improve it neuroplasticity principle

Training that drives a specific brain fxn can lead to an enhancement of that fxn

Specificity neuroplasticity principle

The nature of the training experience dictates the nature of the plasticity

Repetition matter neuroplasticity principle

Repetition of a newly learned behaviour may be required to induce lasting neural changes

Intensity matters neuroplasticity principle

Induction of plasticity requires sufficient training intensity

• If really want to see change need to have intensive block of training - short treatment blocks

Time matters neuroplasticity principles

Different forms of plasticity occur at different times during training

• can be certain windows of times where the brain is more receptive to learning/plasticity

Saliency matters neuroplasticity principles

The training experience must be sufficiently salient/meaningful to induce plasticity

Age matters neuroplasticity principle

Training-induced plasticity occurs more readily in younger brains

• younger brain - is more plastic and better able to respond to damage (advantage)

• Older brains not as plastic  (disadvantage) - plastic potential slightly more challenging

Transference neuroplasticity principles

Plasticity in response to one training experience can enhance the acquisition of similar behaviours

Interference neuroplasticity principle

Plasticity in response to one experience can interfere with acquisition of other behaviours

• plasticity can have negative outcomes