Hypertonia & Ataxia in MS

Management of MS Hypertonia

·         Spasticity

·         Reduction of tone must have a clear objective with an achievable functional benefit

·         High tone is often useful for standing and transferring

·         Some hypertonia can be changeable in distribution, for example lower limb extensors in standing but flexors in lying

·         Where there is a hypertonic muscle, the antagonists are often hypotonic.

·         Imbalances may need to be corrected to avoid contractures and deformity

·         Most common muscle groups are:

·         Trunk rotators

·         Trunk lateral flexors

·         Hip flexors and adductors

·         Knee flexors

·         Plantarflexors

·         Inverters

Types of Ataxia

·         Sensory ataxia

·         High stepping gait pattern

·         More reliance on visual or auditory senses

·         Information about leg or foot position

·         Vestibular ataxia

·         Disturbed equilibrium in standing and walking

·         Loss of equilibrium reactions

·         Wide-based, staggering gait pattern

·         Cerebellar ataxia

·         Disturbance in the rate, regularity and force of mvt

·         Loss of mvt co-ordination

·         Dysmetria (overshooting of target)

·         Dyssynergia (decomposition of mvt)

·         Dysdiadochokinesia

·         Inco-ordination of agonist and antagonists

·         Loss of continuity of muscle contraction (tremor)

Management of MS Ataxia

·         Commonly seen with spasticity

·         Alters the direction and extent of a voluntary mvt

·         Impairs the sustained voluntary and reflex muscle contraction necessary for maintaining posture and equilibrium

·         Inability to make mvts which require groups of muscles to act together at varying degrees of co-contraction, as required during gait as the single stance phase requires co-contraction in order to support body weight whilst shifting body weight forward

·         Walking aids allow the pt to flex at the hips removing the need for co-ordinated change between hip flexion to extension whilst weight bearing on the stance leg

·         Can lead to postural abnormality

·         Exaggerated lumbar lordosis

·         Anterior pelvic tilt

·         Hip flexion

·         Hyperextensive knees

·         Weight shift towards heels

·         Clawed toes

Assessment & Treatment Approached for MS Ataxia

·         Maintaining equilibrium

·         Weight bearing and transference

·         Increase postural stability

·         Control of CoG

·         Differing base of support

·         Co-ordination of dynamic mvt

·         Patterns of mvt

·         Enhance smoothness of control

·         Progress from simple, fast mvts to complex, slow mvts

·         Located in body axis and trunk

·         Gross body mvts ie transfers

·         Independent head mvt

·         Increase control of mvt around the midline

·         Mvt of limb girdles in relation to midline (especially rotation)

·         Located in limbs

·         Voluntary body mvts

·         Enhance proximal limb stabilisation

·         Co-ordinate activity of agonist and antagonists

·         Progress from large to small range mvts

·         Reduce requirement of visual guidance

Multiple Sclerosis

Multiple sclerosis (MS) can present from any age, however has peak influence at 25 – 35 years. The course of the illness is unpredictable, and is twice as common in women as in men. The course of the disease ranges from a single transient neurological deficit with full recovery to permanent disability within weeks or onset. Many people remain mobile and can live a near-normal life.

MS is a demyelinating disease that has immune mediated destruction of myelin as the primary pathological finding, with relative sparing of the other elements of the CNS. It has episodes of acute neurological disturbance, affecting non-contiguous (unconnected) parts of the CNS, are separated by periods of remission. The disease can be progressive in nature and initially, recovery following a relapse is normally complete. However some attacks do not recover completely and leave remains of continuing disability.

Classification

·      Benign MS

·      One or two relapses, separated by some considerable time, allowing full recovery and not resulting in disability

·      Relapsing Remitting MS

·      Characterised by a course of recurrent discrete relapses, interspersed by periods of remission when recovery is either complete or partial

·      Secondary Progressive MS

·      Progressive deterioration after relapses and remissions, with or without identifiable relapses where disability increases even when no relapse is apparent

·      Primary Progressive MS

·      Typified by progressive and cumulative neurological deficit without remission or evident exacerbation

Early Signs & Symptoms

·      Visual loss

·      Double vision

·      Weakness

·      Numbness

·      Imbalance

·      Slurred speech

·      Nystagmus (rapid involuntary mvts of the eyes)

·      Intention tremor

·      Trigeminal neuralgia (intermittent stabbing pain in the face)

Signs & Symptoms During MS

·      Fatigue

·      Optic atrophy

·      Opthalmoplegia, with facial sensory and motor symptoms

·      Cerebellar disease causing nystagmus, ataxia and tremor

·      Hypertonia

·      Spasticity

·      Pain

·      Tremor

·      Weakness

·      Brisk reflexes

·      Impaired walking ability

·      Sphincter disturbances

·      Psychiatric and psychological disturbances

·      Possibly epilepsy (generally focal)

Symptoms are exacerbated by heat and cold.

Physiotherapy Interventions

·      Stretching

·      Reduce hypertonia

·      Active exercise

·      Retraining function

·      Muscle strengthening

·      Retraining of balance and co-ordination

·      Maintaining ROM

                           Therapeutic exercises causing fatigue were widely thought to be damaging and the consensus is that moderate exercise is appropriate but that too much, which precipitates fatigue, is too much. Exercises can lead to worsened motor impairments, however leads to significantly less deterioration.

                           Weight-resisted exercises are deemed inappropriate.

                           Aerobic exercises aim to increases overall physical activity and cardiovascular effort, prevent general muscular weakness and reduce health risks due to deconditioning and disuse.

·      Walking aids

·      Aims to maintain ambulation

·      Need to avoid postural instability and deformity with long term use

·      Hydrotherapy

·      Inconclusive. Similar argument to on land exercises.

·      Heat & cold

·      Heat aids muscle stretching exercises

·      May exacerbate clinical and subclinical deficits

·      Cold could further compromise circulation with vasoconstriction

·      Electrotherapy

·      As an adjunct to active exercise and stretching

·         Is not suitable for all MS patients

Parkinson's Disease

Diagnostic Signs:

• Resting tremors
• Rigidity – lead pipe and cog wheel (catches)
• Bradykinesia – slowness of movement
• Caused by a loss of dopamine in the basal ganglia.

Akinesia – no movement   
Hypokinesia – reduced, small movements

Clinical Features:

• Festinating gait (increased speed shuffle)
• Postural problem
• Loss of facial expression
• Altered speech
• Depression
• Difficulty Swallowing
• Sleep disturbance
• Pain

Secondary Impairments

• Falls (inc. fear of)
• Weight loss
• Reduced ROM
• Muscle weakness
• Social exclusion
• Fatigue
• Infections (esp. chest)
• Balance issues

Assessment

• Current medication
• Certainty and date of diagnosis
• Hoehn and Yahr stages and UPDRS
• Symptoms
• Observation
• Walking
• Dual task eg carrying & walking
• Fall History inc. fear of falling
• Two thirds of PD patients fall each year
• Location
• Activity and suspected cause
• Saving reactions/landing

Treatment

This is mainly L-dopa as it is small enough to cross the blood brain barrier. It works fantastically in new patients, but the effect fades. It creates on-off phases depending on the timing of the dosage.

Cueing

This is what is used to bypass the dopamine system. It is the use of a response to a stimulus.

Visual – lines on the floor/signs

Auditory – metronome or instructions

Proprioceptive – conscious movement to break freeze

Cognitive – focus on movement, really think about it

Physiotherapy for 2 -3 times a week for 4 – 12 weeks, including a follow up.

Stroke

A stroke is a blood clot in the brain that deprives an area of blood carrying oxygen. WHO defines stroke as ‘an acute deficit resulting from vascular disease that lasts for more than 24 hours.’ If it less than 24 hours it is a Transient Ischaemic Attack (TIA).

The most improvement in strength within the first month is observed in the first 48 hours, hence Hyper Acute Stroke Unit (HASU) for the first 72 hours. There are 67,000 deaths in England and Wales with 300,000 people living with a stroke.

Ischaemia – a deprivation of oxygen

Risk Factors

• Age
• Hypertension
• Ischaemic Heart Disease
• High blood cholesterol
• Genetic predisposition
• High salt level
• Smoking
• Diabetes mellitus
• Atherosclerosis
• Alcohol consumption

It can accumulate over 2 years with small blood clots at the ends of vessels that give similar symptoms to going senile.

Types of Stroke

Ischaemic Stroke – this is the slow onset of a thrombosis and accounts for 85% of strokes. It is embolic – there is a blockage of arterial access by an embolus which is a travelling particle.

Haemorrhagic Stroke – this is rapid onset and accounts for 15% of strokes with 2 categories. The first being subarachnoid which is where blood flows into the subarachnoid space, usually resulting from a ruptured aneurysm. The second is intracerebral which is where the lumen narrows leading to microaneurysms (little bubbles).

Ischaemic Punumbra – an area of vulnerable cells surrounding the core ischaemic area.

Ischaemic Cascade – a decrease in O₂ levels  an increase of lactate  no Na⁺ + K⁺ pump. This means there is an influx of calcium that allows no synthesis and deactivation of enzymes.

Hemispacial Neglect – inability to pay attention to stimuli on contraside of damaged hemisphere. This is generally in the parietal and temporal lobe and two thirds of this type are affected.

Guillain-Barre Syndrome

Guillain-Barre Syndrome (GBS), also known as acute inflammatory demyelinating polyneuropathy, is an autoimmune disease whereby antibodies mistake the myelin sheath for pathogens. This results in demyelination of the peripheral nerves and nerve roots leading to muscle weakness. It commonly follows a respiratory tract or gastric infection, or perhaps from immunisation or surgery. In order to be classified as GBS, the time of onset to peak disability (nadir, meaning opposite or lowest point in fortunes) should be less than 4 weeks. 

Muscle Weakness

·  Leg weakness if often noted first, progresses proximally and includes all muscle groups

·  Asbury & Corblath (1990) discovered that 50% of pts reach nadir in two weeks

·  Nadir can include complete paralysis, and 50% of pts have facial weakness

·  Frequently bulbar muscle groups are affected to require NG feeding to avoid aspiration

·  Paralysis of respiratory muscles causes vital capacity to fall in 30% of pts, where elective ventilation is indicated

GBS is predominantly a motor neuropathy, but 42-75% of pts have some alteration in sensation. Joint positional sense in the toes is missing in over 50% of pts. It has been postulated that pain could be due to inflamed and tightened neural structures in the acute stage, however could be due to abnormal forces on joints that are poorly protected by weakened muscles.

Recovery tends to occur within a month of nadir, and has the potential to be complete providing secondary implications such as contractures are avoided.