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. 

Sprains

Early Management Aims during the first 72 hours

• Reduce tissue temperature, pain and swelling
• Reduce metabolic demands of the tissue
• Prevent further injury
• Promote collagen growth and realignment
• Maintain cardiorespiratory and musculoskeletal activity

Acute Inflammatory Stage - PRICE

Protection - Prevents worsening of injury
Rest - Avoids pain from movement. Complete immobilisation is not indicated to prevent significant loss of ROM. Even for grade III injuries a functional splintage is strongly suggested.
Ice - Reduces pain. Application of ice should be for 10-30 minutes wrapped in cloth to avoid cold injury. Repetition can be as frequent as required, providing the affected part is fully warmed back to body temperature.
Compression - Provides comfort by limiting movement and reducing swelling, although should be applied so as to not reduce blood flow. 
Elevation - Helps to reduce swelling, especially with the affected part above heart level.

Sub-Acute Proliferation & Remodelling Stage

Active rehabilitation:

• Electrotherapy (for example ultrasound for collagen synthesis)
• Manual therapy (for joint pain)
• Restore mobility and prevent joint deformity
• Progressive loading to begin to restore strength and improve joint stability

In the remodelling stage:

• Deep tissue frictions
• Electrotherapy (for example ultrasound to enhance tensile strength and scare mobility)
• Manual therapy (for joint stiffness)
• Progressive mobilisation and strengthening exercises

Soft Tissue Healing

A soft tissue injury is the damage of muscles, ligaments and tendons throughout the body when their tensile strength is interrupted. They normally result in pain, swelling and bruising as well as loss of function.

Tissue healing compromises two essential components: regeneration and repair (dependant on the resultant tissue). In regeneration specialised tissues is replaced by the proliferation of surrounding undamaged specialised cells. In repair, lost tissue is replaced by granulated tissue which matures to form scar tissue.

The healing process is divided into 4 phases: bleeding, inflammation, proliferation and remodelling. These 4 phases hugely overlap and integrate during repair.

Bleeding is a relatively short phase that occurs following trauma or another similar insult. The normal time for bleeding to stop varies depending on the injury and the tissue type. Vascular tissue such as muscle will bleed for longer causing a greater escape of blood into the surrounding tissues whereas other tissues such as a ligament will bleed less and for a shorter amount of time. The average bleeding time is 6-8 hours although is heavily dependent on the patient and the nature of the injury, for example a crush injury to a vascular tissue could continue bleeding, admittedly minimally, for 24 hours post trauma.

Inflammation is a normal and necessary prerequisite to healing (Hardy 1989) and onsets after a few hours. It rapidly increases in magnitude over the following 1-3 days before gradually resolving over the following couple of weeks. Signs of inflammation include: swelling, pain, redness, heat and loss of function.

The cascade that is responsible for the initiation and control of inflammation can be due to trauma, mechanical irritation, thermal or chemical insult as well as immune responses. Fibrin and fibronectin form a substratum (underlying foundation layer) which is hospitable to the adhesion of various cells. The two essential elements to inflammation are the vascular and cellular cascades. They occur in parallel and are somewhat interlinked.

Vascular events are additional to the initial bleeding. Vasodilation follows an initial brief vasoconstriction and there is an initial increase in the velocity of the blood followed by a prolonged slowing. The white cells form a margin, platelets adhere to the vessel walls and the endothelial cells (lining the blood vessels) swell. The local vessels also become more permeable, which when combined with vasodilation, increases the flow of blood through the more permeable vessels and results in exudate (including protein rich plasma) passing into the tissue spaces. This can be at both the arterial and venous ends of the capillary network as the increase hydrostatic pressure overcomes the osmotic pressure of the plasma proteins.

The effect of the exudate is to dilute any irritant substances in the damaged area and form a fibrin clot with the high fibrinogen content of the fluid. This union between the surrounding intact tissues forms a mesh which can trap foreign particles and debris. Mast cells in the damaged area release hyaluronic acid and other proteoglycans which bing with the exudate and create a gel which limits local fluid flow and further traps various particles and debris (Hardy 1989).

The cellular events of inflammation include the early emigration of the phagocytes within minutes. They are followed out of the vessels by monocytes, lymphocytes, eosinophils and basophils (Lorena et al 2002). Once in the tissue spaces monocytes become macrophages (Forrest 1983). These cells exhibit a strong phagocytic activity and are responsible for the removal of damaged tissue and foreign objects. And to top it all off lactic acid, one of the end products of phagocytosis, is a stimulant for proliferation. Pretty clever, ‘ey? Increased hydrostatic pressure for the oedema can be detrimental as it can restrict blood flow if the injured tissue space is limited, increasing pain and limiting function.

Proliferation is the generation and deposition of granulation (repair) tissue, which in the majority of musculoskeletal injuries is collagen (scar) material. It has a rapid onset of 24-48 hours but takes 2-3 weeks to reach its peak reactivity, although the more vascular the tissue the shorter the time taken to reach this peak phase. The bulk of the scar production is completed during this time, but proliferation decreases thereafter through several months post injury. The key events in proliferation are: fibroplasia (production of fibrous tissue), angiogenesis (development of blood capillaries), increased extracellular collagen production, wound contraction (from myofibroblasts) to minimise the scar and a complex interactive response amongst cells and chemical mediators to ensure effective completion of the scar tissue.

Remodelling is the strengthening (type I collagen replaces type III) and alignment of collagen that results in an organised, quality, functional scar that allows movement in a similar way to the original tissue. This phase is widely reported to begin at the same time as the peak of the proliferative phase (2-3 weeks) however further research shows that it may begin at around 1-2 weeks post injury. During this phase movement is essential to ensure that the collagen aligns in the direction most suited to functional activities. Signs of the remodelling phase include reduced redness, oedema and pain.

Factors that are known to delay healing can be general or local. General factors include age, protein deficiency, low vitamin C levels, steroids and NSAIDs as well as cold temperatures. Local factors include ischaemia, adhesion to bone of other underlying tissue, continued inflammation, drying of the wound and excessive movement as it restarts inflammation.

Leg Length Discrepancy

Having worked in a ski resort for the last 5 months, I have been in the unique position of only being able to see clients for the duration of their holiday. This means I have encountered a number of people who have been seeing the same therapist, at home, for a period of months to years. This has led me to one shocking revelation:

so many people don't know their own diagnosis

...and yet they continue to see their therapist. Does it not seem crazy that most of these clients cannot state what their therapist has been treating?! From these clients, the best I hear is nearly always 'My hips are out of alignment' or 'I've got one leg slightly shorter than the other.' Well... so what?

Gurney (2002) reviewed leg length discrepancy and suggested it does not need treating in all cases, with 20mm often used as the 'breakpoint'. Two centimetres! That's not a small amount. Furthermore, Gross (1978) conducted a survey in which all patients with a leg length discrepancy between 15 and 20mm 'did not consider their short leg to be a problem in any way.'

Based on a review published in 2005, 90% of the population has some anatomic leg length discrepancy (average 5.2mm), although this figure hugely varies between studies. Seven of the studies reviewed identified whether participants were symptomatic (LBP or knee/hip problems) or asymptomatic (varying from last 6 months to ever) ...and guess what? The mean leg length discrepancy between the two groups differed by 0.1mm (symptomatic mean 5.1mm, SD 3.9; asymptomatic mean 5.2mm, SD 4.2).

This isn't new information. The studies used in the above review were conducted between 1970 and 2005. Soukka et al (1991) measured leg length using radiographs in 247 participants between the ages of 35-54 years. 78 of these participants had disabling low back pain during the previous twelve months and a mean leg length discrepancy of 5.3mm (maximum 17mm). However, a further 53 participants also had a discrepancy (mean 5.5mm, maximum 20mm) but... wait for it... absolutely no history of low back pain.

Then, in 2006, 126 of 1,100 military cadets were identified to have lower limb discrepancy over 0.5cm. Over the following year there was no difference in incidence of injury between those with discrepancies and those without (Goss et al, 2006). Furthermore, gait asymmetry and effects on kinetics and kinematics are only present in discrepancies over 2cm (Kaufman et al, 1996).

Furthermore, accurate measurement of a leg length discrepancy requires the use of radiographic imaging.

However, amongst these studies, there is evidence that leg length discrepancies are linked to increasing your chances of some injuries. Lower limb stress fractures have been shown to be of higher incidence in those with discrepancies. This is also true of trochanteric bursitis, patellar apicitis, and patellofemoral syndrome amongst many others. However, there are also studies that state leg length discrepancies have little to no effect. And on an interesting side note, there are differing conclusions as to whether leg length discrepancies would predict or be the result of knee and hip OA (intriguingly this is predominantly in the longer leg, rather than the shorter).

Basically, there remains huge debate as to the effects and clinical relevance of leg length discrepancy. It is logical for there to be pelvic torsion when one leg is longer than the other, however there is inconclusive evidence to use leg length discrepancy and hip misalignment as a diagnosis for pain - especially for an acute issue. If using leg length discrepancy as a diagnosis, why not investigate whether there is piriformis malfunction, OA, plantar fasciitis or one of the many other questioned associated pathologies? With treatment for leg length discrepancy (such as foot lifts or surgery) recommended only for those with >2cm difference, manual therapies and exercise prescription are commonly looked to for those with <2cm difference. Clients should be questioning exactly how manual therapies are going to benefit their leg length discrepancy, or whether therapy is instead for an effect of their leg length discrepancy (that is, if the issue is related at all).

References

Goss, D. L., Moore, J.H., Slivka, E. M. and Hatler, B. S. (2006) 'Comparison of injury rates between cadets with limb length inequalities and matched control subjects over 1 year of military training and athletic participation' Military Medicine 171(6), pp. 522-525.

Gross, R. H. (1978) 'Leg length discrepancy: how much is too much?' Orthopedics 1(4) pp. 307-310.

Gurney, B. (2002) 'Leg length discrepancy' Gait & Posture 15 pp. 195-206.

Kaufman, K.R., Miller, L.S., Sutherland, D. H. (1996) 'Gait asymmetry in patients with limb-length inequality' Journal of Paediatric Orthopaedics 16 pp. 144-150.

Knutson, G. A. (2005) 'Anatomic and functional leg-length inequality: A review and recommendation for clinical decision-making. Part I, anatomic leg-length inequality: prevalence, magnitude, effects and clinical significance' Chiropractic & Osteopathy 13(11)

Soukka, A, Alaranta, H, Tallroth, K and Heliovaara, M (1991) 'Leg-Length Inequality in People of Working Age: The Association Between Mild Inequality and Low-Back Pain Is Questionable' Spine 16(4).