Week 12 Cue Cards

cellular responses to injury in the CNS

• The CNS responds to injury at a cellular level through physical changes in response to disease states.

• Key descriptors of neuropathology will be discussed, including:

  • The physical and physiological changes that occur.

  • Pathological alterations leading to symptoms cannot often be recognised with the naked eye, necessitating further examination (CAT scan, lab tests, microscopic analysis).

• Morphological changes in reaction to pathology provide clues regarding the underlying cause.

classification of neurological disorders

Primary vs. Secondary Disorders

• Primary Neurological Disorders: Affect the brain, spinal cord, and peripheral nerves directly and are not caused by another condition. Examples:

  • Dementia

  • Stroke

  • Parkinson's Disease

  • Epilepsy

• Secondary Neurological Disorders: Develop due to extra-neural disorders such as injuries or infections that lead to complications. Example:

  • Headaches after stroke or brain tumour.

• Differentiation in regenerative capabilities between CNS and peripheral nervous system (PNS).

  • CNS has limited regenerative capability due to inhibitory factors.

  • PNS can regenerate more effectively due to supportive cells (Schwann cells).

neuroplasticity in CNS

• While CNS typically does not self-repair after injury, neuroplasticity allows for reorganization which is crucial during rehabilitation.

inhibitory factors in CNS repair

• Factors that hinder axon regrowth in CNS include:

  • Scar formation in glial cells

  • Various inhibitory substances that promote long-term recovery obstacles.

brain oedema

• Definition: Swelling of brain tissue due to excess fluid accumulation, leading to increased intracranial pressure (ICP).

• Typical causes of brain oedema:

  • Traumatic brain injury

  • Haemorrhagic stroke

  • Tumours

  • Infections

• Symptoms of brain oedema:

  • Dizziness

  • Headaches

  • Altered consciousness

  • Seizures

• Normal ICP ranges from 8 to 15 mmHg, with risks increasing above 20 mmHg leading to cerebral ischemia.

• ICP is affected by:

  • Blood volume,

  • Cerebrospinal fluid volume,

  • Brain tissue volume.

brain herniation

• Definition: Displacement of brain tissue caused by increased ICP, often following trauma or haemorrhagic stroke.

• Symptoms include:

  • Headaches

  • Nausea

  • Dilated pupils

  • Loss of consciousness

• Cushing's triad (increased blood pressure, irregular breathing, bradycardia) indicative of imminent herniation.

hydrocephalus

• Definition: Accumulation of cerebrospinal fluid (CSF) within brain ventricles.

• Symptoms may include:

  • Headaches

  • Dizziness

  • Vomiting

• Treatment often involves surgery to restore CSF flow (e.g., VP shunt).

neuronal injury responses

Cell Death and Changes

• Necrosis: Death of neurons due to irreversible injury.

• Apoptosis: Programmed cell death, leads to cell shrinkage.

• Central Chromatolysis: Swelling of the cell body and displacement of the nucleus in response to injury.

• Wallerian Degeneration: Breakdown of axons distal to injury, occurring post-injury in both CNS and PNS.

Neurofibrillary Degeneration

• Abnormal aggregation of tau proteins leading to tangles in neurons; notable in Alzheimer's disease.

cellular responses by glial cells

Changes in Astrocytes

• Astrogliosis: Increase in size and number of astrocytes in response to injury, correlating with swelling.

• Rosenthal Fibres: Identified in gliomas, indicate low-grade tumours.

Role of Microglia

• Act as the immune response in the CNS, removing debris and initiating responses but can also cause secondary damage with chronic activation.

Oligodendrocytes and Myelin Damage

• Damage to oligodendrocytes leads to demyelination, impeding signal transmission.

Clinical Presentation of Neuropathology

• Symptoms include:

  • Cognitive changes (memory loss, confusion)

  • Motor issues (weakness, tremors)

  • Sensory disturbances (numbness, tingling) 

Diagnosing neuropathologies

• Diagnosis often involves a process of elimination:

  • Focal, multifocal, or diffuse injuries.

  • Classification of injury as acute, subacute, chronic, transient, progressive, or stable.

7 main types of pathological changes 

1. Degenerative Disorders: Neuronal dysfunction, progressive loss, often with misfolded proteins (e.g., Alzheimer's, Parkinson's).

2. Neoplastic Diseases: Brain tumours, incidence approximately 21 per 100,000 people/year, typically do not metastasise.

3. Vascular Diseases: Tissues at risk from oxygen deprivation, leading to infarcts or haemorrhages.

4. Inflammatory Diseases: In response to microorganisms or toxins, can result in abscess formation - treat promptly to minimise damage.

5. Immunologic Diseases: Autoimmune responses attacking CNS (e.g., MS, Guillain-Barre Syndrome).

6. Toxic Metabolic Diseases: Result from toxins or nutritional deficiencies; can lead to widespread neurological damage.

7. Traumatic Diseases: Result from external forces, often leading to immediate and potential long-term symptoms such as depression and personality changes.

transient disorders and system-level disorders

• Transient Disorders: Temporary problems affecting brain control over motor systems, strength, sensation, etc. Can lead to things like transient ischemic attacks (mini strokes) or migraines.

• System-Level Disorders: Broader conditions such as stroke, MS, Alzheimer's; typically exhibit diverse symptoms based on underlying pathology.

fronto-parietal region function

-        Sensory

-        Decision making

-        Personality

-        Cognition

-        Preplanned movements

-        Modulation, coordination, attention

cerebellar region function

coordination issues, ataxia, poor trunk tone, difficulty with consolidating motor learning

medulla region function

near brain stem: respiratory (regulation centre [involuntary]), BP, HR, coughing, sneezing, vomiting

-        May see nystagmus (eye twitches), issues with speech and swallowing

posterior parietal function

-        Speech/language

-        Spatial awareness

-        Loss of proprioception

-        Impaired executive functions

-        Visual disturbance

occipital lobe

-        Visual field deficits

Prosopagnosia (ability to recognise someone’s face) (facial blindness)

examples of sensory and motor impairments

Impairment	Classification	Rationale
L hemiplegia (weakness L UL/LL)	Motor	Reduced activation and muscle strength post R MCA stroke
Left neglect	Perceptual (sensory-integration)	Impaired spatial awareness and attention to the left side
Left homonymous hemianopsia	Sensory (visual field loss)	Visual pathway disruption
Impaired tactile sensation and proprioception (L side)	Sensory	Reduced somatosensory input
Reduced balance / inability to ambulate	Motor (plus sensory contribution)	Weakness and impaired postural control
Falls risk	Motor + sensory + cognitive	Impaired motor activation, poor insight, perceptual loss
Diminished tone and DTRs L side	Motor	LMN characteristics in acute stage of UMN lesion
Cognitive impairments (STM deficit, orientation issues)	Cognitive	Likely related to premorbid dementia and stroke

assessment choices

Motor Impairments

• MMT for gross strength (simple and familiar)

• Functional observation during transfers and sitting balance

• Motor Assessment Scale (MAS) for hemiplegia

• Trunk control assessment (e.g., Trunk Impairment Scale elements)

Sensory Impairments

• Light touch, proprioception, and stereognosis testing on L UL/LL

• Functional sensory integration assessment during tasks such as reaching

• Visual field confrontation test to identify hemianopsia

Perceptual Impairments

• Albert’s Test for unilateral neglect

• Line bisection task if attention allows

• Observation during functional tasks to determine real-world impact

Balance and Mobility

• Bed mobility and transfer analysis

• Sitting balance tests given inability to stand unsupported

• Vital signs monitoring due to fatigue and deconditioning

Cognitive Function

• Orientation questions

• Short-term memory recall tasks

• Behavioural observation during repeated instructions

specific outcome measures and their justification

Outcome Measure	Justification
Fugl-Meyer Assessment (FMA)	Comprehensive quantitative measure of motor recovery post-stroke, including motor, sensory, balance, and reflex components. Suitable for early and severe deficits.
Motor Assessment Scale (MAS)	Tracks functional mobility improvements specific to hemiplegia, including transfers and sitting balance. Feasible in inpatient rehab.
Functional Independence Measure (FIM) / or UK equivalent (e.g. Barthel Index)	Captures progress toward activities of daily living and discharge readiness. Relevant for safety planning and home environment constraints.
Catherine Bergego Scale (CBS)	Functional measure of neglect impacting daily performance. Complements visual scanning assessments.

addressing motor weakness and impaired sensation

o   Motor weakness (dense L hemiplegia)

§  Improve motor activation, functional strength, and early postural control

§  Repetitive training for bed mobility and transfers (supine to sit, sit to stand) with graded assistance.

§  Early WB through L LL during standing practice with therapist support

§  Tactile input, tapping, or NMES for muscle activation of key muscle groups

o   Impaired sensation and proprioception (left side)

§  Improve sensory awareness and integration to support functional movement

§  Sensory re-education: tactile discrimination tasks, textured object handling, proprioceptive loading in sitting and standing

§  Mirror therapy targeting motor imagery and visual compensation for reduced sensory feedback

§  Joint compression activities to improve limb awareness and control

addressing impaired perception and cognition

o   Perceptual deficits (left neglect + left homonymous hemianopsia)

§  Increasing scanning, attention, and engagement with left hemisphere

§  Visual scanning training with cues placed in left field

§  Anchoring and environmental modifications (mirrors, contrasting tape)

§  Bilateral task training to encourage use of the left arm or attention to the left side

§  Education for staff and family on cueing strategies to reduce falls and safety incidents.

o   Cognitive impairments (STM, orientation)

§  Enhance safety, engagement in rehab, and learning retention

§  Clear, simple and repeated instructions during tasks

§  Use of orientation boards, written schedules, and memory aids

§  Maintain consistent routines to strengthen procedural learning

§  Break tasks into manageable steps to reduce cognitive load

addressing impaired mobility and hypermobility

o   Functional mobility limitations and falls risk

§  Improve independence in transfers and sitting balance while reducing falls risk

§  Progressive sitting balance and edge-of-bed activity

§  Transfer practice using mechanical lifter initially, then transition to assisted pivot transfers when safe

§  Education on safety awareness to prevent impulsive attempts to stand

§  Early gait initiation with appropriate support when medically and physically appropriate

o   UL Hypertonia Risk and hypermobility (L UE)

§  Protect joint integrity and prevent secondary MSK complications

§  Safe positioning of limb in bed

§  Use of slings

§  Gentle supported AROM and functional reach tasks as motor return emerges

§  Family education on handling techniques

addressing deconditioning and incontinence

o   Deconditioning and low activity tolerance

§  Improve CVS and muscular endurance

§  Short but frequent therapy sessions

§  UL and LL ergometry on the unaffected side to maintain fitness

§  Gradual increase in unsupported sitting time and static standing tolerance

o   Incontinence management and skin protection

§  Regular toileting schedule

§  Pressure area protection

§  Monitor stroke related bladder dysfunction

more outcome measures

Outcome Measure	What it Assesses	Rationale for Use in This Case
UPDRS – Motor Section (Unified Parkinson’s Disease Rating Scale)	Overall motor function: rigidity, tremor, bradykinesia, posture, gait	Gold-standard PD assessment; captures core motor impairments
Sit-to-stand Test (5x STS)	LL strength and functional transfer ability	Assesses bradykinesia, strength, and postural control during transfers
Timed Up and Go (TUG)	Functional mobility, sit-to-stand, gait speed, fall risk	Sensitive to mobility deficits, freezing, and dual-task impairments
Mini-BESTest	Dynamic balance and postural control	Sensitive to balance deficits and fall risk in PD; evaluates anticipatory and reactive balance
Berg Balance Scale (BBS)	Static and dynamic balance, falls risk	Relevant due to imbalance, shuffling gait, and fall history; validated in PD
10-metre walk test (10MWT)	Gait speed and walking efficiency	Short, practical measure of walking ability, sensitive to PD-related gait changes
Functional reach test (FRT)	Dynamic balance and fall risk	Assesses forward reach, postural control, and fall potential in PD
6-minute walk test (6MWT)	Walking endurance	Assesses functional gait capacity and endurance