Physical Therapy intervention in PD :Part 2.

3.BALANCE TRAINING : 
The balance training program is extremely beneficial for regaining the independence of the patient , to reduce the fear of falling and hence , reducing the fall episodes.
 The training should include a tailor-made simulative method by trying to duplicate the conditions the patient encounters everyday.
 There have to be clear and precise instructions from the therapist like ,"sit erect" or "stand tall"
 -stability tasks
weight shifts , reach-outs, axial rotation of head and trunk , axial rotation combined with functional reaching , etc.
 -seated activities
sitting on therapy ball or an inflatable discs , which is unstable and hence, motivates the patients to maintain balance.
-transitions
 from sit to stand , stand to sit , sit to lying supine and vice versa.
 -challenges
 voluntary movements while trying to balance, reduced lighting, open environment,etc
 Later, progression to dynamic activities can be made .
 Frenkel's exercises can also be used for balance training.

 4.LOCOMOTOR TRAINING: 
The focus of this training revolves around the obvious gait impairments like slow speed, reduced arm swing, stooped posture while walking , etc.
 These flaws can be corrected by firstly improving the dynamic balance and posture , then widening the Base of Support (BOS) , increasing the arm movements and increasing speed.
Proper visual and auditory feedback should be given to encourage the patient.
 Some stretegies include -
 -practice marching in place
 -lift the toes while walking
 -spread the legs to increase the BOS
-use smaller steps while turning
 -while experiencing a freezing episode , lift the toes off the ground


 5 CARDIOPULMONARY TRAINING:
 L-dopa can produce orthostatic hypotension and arrythmia.
Besides, any respiratory dysfunction leads to increased morbidity and mortality rates.
This can be commonly found in patients with PD because of the flexed posture and hence, reduction in lung expansion.
The following methods can be taught-
-deep breathing exercises
 -diaphragmatic breathing
 -maintained trunk extension
-aerobic training

Physical Therapy intervention in PD :part 1.

PHYSICAL THERAPY INTERVENTION

1.MOTOR LEARNING TECHNIQUES:
Patients with PD have difficulty in performing complex tasks involving long sequential movements.So basically the movements have to be simplified for the patient's convinience . External cues or commands have to be given to the patient.A simple instruction is very beneficial because it improves patient's attention .It bypasses the internal cueing of basal ganglia which is faulty.Visual cues like floor markings , or auditory cues like short verbal instructions, tactile cues by touching or even multisensory cues (auditory&visual) are very effective. They reduce the freezing episodes.
A very important aspect is repititions.A long sequential movement is broken down and the parts is repeated frequently with proper instructions.

2:EXERCISE TRAINING:
a-Relaxation exercises:
 Relaxation is needed to reduce the tension developed in muscles due to rigidity.Gentle and slow rhythmic movements of extremities and trunk should be considered before stretching and functional training.The PNF technique of rhythmic initiation can be used. 
This begins as a passive movement and progresses to active assisted, active and finally resistive movement.This helps to overcome rigidity.
Breathing exercises like diaphragmatic breathing should be taught as breathing promotes relaxation.
Sustained steady stretching can begiven to reduce rigidity


 b-Flexibility exercises: 
Flexibility is improved by giving passive movements initially and progressing to active movements or range of motion(ROM) exercises.This helps to lengthen the short flexor muscles and strengthern the elongated extensor muscles.Hold-relax and contract-relax methods of PNF can be used.
Traditional stretching techniques with joint mobilzation can be used whie maintaining the stretch for atleast 15-30 seconds.
Passive positioning in prone lying can be given to counteract the acquired 'phantom-pillow' posture in supine.Trunk extension should be done to oppose the kyphosis and hip-knee extension should be maintained to prevent adducted and flexed posture.


 c-Strength training:
Patients demonstrate typical disuse atrophy of muscles and weakness.And this leads to stooped posture, postural instability and frequent falls.Strengthening exercises show good improvement in patients with mild to moderate PD.Strength training along with balance training is effective .It includes high intensity resistance training for lower extremities.The strength training can be timed with the L-dopa for optimum results when the drug is administered .Not much effect can be expected during the off period of the drug.Training during 1 hour after the drug is taken is helpful.


 d-Functional training:
 The exercise training should focus on functional training. This helps to make the patient become independent in his daily activities.
Specific emphasis should be laid on improving the mobilitty of axial structures like the neck , the trunk, shoulders and hips. Bed mobility should be taught,focusing on rolling, supine to sitting,etc.Segmental rolling is better than complete rolling.This can be practiced on different surfaces , progressing from firm to soft.
Using the therapy ball, the patient can be taught anterior and posterior tilts, side-to-side tilts,and pelvic clock exercises.these activities can then be progressed to a firm surface like a mat or plinth.
Sitting activities can be taught using PNF patterns UE D2F and D2E .They promote upper trunk extension
Gentle rocking movements have been proven beneficial to induce a desired movement keeping the body relaxed. eg, sit to stand.
Standing in a modified plantigrade position improves stability.
Once the patient learns how to balance while standing, then rotational movements of the trunk can be practiced.
Due to the tendency of fall in PD patients, they should be taught how to get up on their own after an episode of fall.quadruped creeping to kneeling , half kneeling and finally standing should be taught.


e.Adaptive and supportive devices:
The following devices and modifications will help the patient to regain mobility,stability and support:
-elevated head of the bed
-a rope tied to the end of the bed to pull onto while getting up
-high sitting chairs and sofas
-rocking chair
-a cane or walker (without wheels)
-reachers (to grab things)
-loose fitting clothes
-sneakers with velcro , with a raised heel .

Parkinson's Disease : diagnosis and PT assessment

DIAGNOSIS:a diagnosis of PD can be made only if 2 or more cardinal features are present.
Exclusion of parkinson-plus syndromes is necessary and can be done by observing bilateral symmetry in the symptoms and no response to L-dopa. As these are the differentiating factors between the two.
MRI using chemical markers , PET scan and SPECT scan are done.

MEDICAL MANAGEMENT: there is no absolute cure for PD.
Neuroprotective  monoamine oxidase inhibitors(MAOs) like seligiline are administered to facilitate metabolism of intracerebral dopamine.
Seligiline also shows symptomatic relief .If given in combination with L-dopa ,dose can be lowered.

Symptomatic treatment:
1:levodopa-(L-dopa) is the mainstay for symptomatic treatment.It is a precursor of dopamine and is able to cross the blood brain barrier .It corrects the neurochemical imbalance by increasing the level of dopamine in basal ganglia.This drug is however metabolised to a great extent before reaching the brain so higher dosage has to be administered.But that can be changed if carbi-dopa is given along.Sinemet is the common levodopa/carbidopa combination.It reduces bradykinesia and rigidity.There is an initial 'honeymoon' phase where dramatic improvement is seen with the therapeutic window of 5-7 years before the optimal effect wears off.Wearing off phase shows worsening of symptoms. Deprenyl can be given with L-dopa to control it.

 2:Dopamine agonists-administered along with L-dopa so that lower doses can be administered with effectiveness .This is also known as  L-dopa sparing therapy.They reduce rigidity and bradykinesia.
eg.bromocriptine(parlodel),ropinirole(requip)

 3:Anticholinergic agents-given with L-dopa as an early therapy to reduce tremors and rigidity and to smooth motor fluctuations.
eg.benztropine(cogentin),ethoprppazine(parsidol).amantadine also has antiparkinson effects.


SURGICAL MANAGEMENT:
ablative surgery, deep brain stimulation and neural transplantation can be done.


 PHYSICAL THERAPY ASSESMENT: a PT should remember that a patient on L-dopa therapy may demonstrate fluctuations. Good results are obtained in the initial phase whereas results may worsen in the wearing-off phase.A comprehensive evaluation is required to determine the level of impairment of the functions:

1.Posture : posture is invariably affected . It can be graded using a pictorial grading method , on a scale of 1 to 4.
1=normal.
2=with head protruding.
3=head protruding ,with marked kyphotic thoracic spine,slight flexion at knees and elbows.
4=marked flexion of the trunk, elbows,hips and knees.

2.Balance: can be checked using Berg-balance scale , or, ask the patient to -
-sit unsupported for 1 minute
-stand unsupported  for 5 seconds
-stand on one leg and then the other for 5 seconds without an aid.

3.Gait : gait should be assessed by asking the patient to walk a fixed distance. All the parameters like step length, stride length, cadence, etc should be measured. Time taken to walk should also be recorded.

4.Functional assessment: difficulties to carry out essential movements should be assessed. eg, turning in bed ,  lying to sitting,  sit to stand, stand to walk  ,etc. the grading scale used is :
1-normal
2-completes a task with difficulty , but without help.
3-can complete a task with use of an aid , like pulling on the side of the bed.
4-unable to complete the task.

Hoehn and Yahr scale should be used to determine the severity of the disease.
This assessment is done in addition to the routine assessment for neurological conditions.

Parkinson's Disease: clinical features

CARDINAL FEATURES 

1:RIGIDITY -rigidity is nothing but increased resistance to movements by both , the agonist and antagonist muscle groups.It is one of the 4 cardinal features of PD. Patient complains of stiffness or heaviness of limbs.Rigidity is asymmetrical in the beginning , affecting only the proximal muscles.It may begin from shoulders and neck , gradually spreading to face and the extremities.It may be of either types-
cogwheel (jerky resistance on movement due to alternate contraction and relaxation of muscles)
or leadpipe (sustained resistance).
Rigidity increases as the patient tries to actively move or is under emotional stress.
Complications of rigidity are decreased range of motion, contractures  and postural deformity.It increases fatigue levels by increasing the resting energy-expenditure.Objective findings are reduced bed mobility and loss of reciprocal arm swing while walking.

 2:BRADYKINESIA-it means slow and difficult voluntary movements. The speed and amplitude of movements is reduced.All of this leads to increased dependence and poor quality of life of the patient.

 3:TREMORS-involuntary oscillations of body parts occuring at a frequency of 2-4Hz is called tremor.Presence of resting- tremor is an initial and a typical symptom of PD.This kind of tremor appears only at rest and disappears as the patient does an active movement.Tremor tends to be less severe if the patient is relaxed,and aggreviates on emotional stress and fatigue.Objectively it appears as a pill-rolling movement of fingers, supination-pronation of forearm,etc

4:POSTURAL INSTABILITY-affected posture and balance is observed in the later stages of PD.This happens due to rigidity , loss of ROM and weakness.Subjectively , the patient notices loss of balance when his/her attention is divided when he/she is performing a self initiated movement like walking.A flexed , stooped posture with bent hips and knees is commonly seen.Frequent falls are common due to loss of balance as the patient cannot quickly adapt to changing sensory conditions.Fear of falls, freezing and fatigue are yet other symptoms . Freezing refers to the rigidity that the patient experiences , which in turn leads to complete inability to move that particular part.for instance, legs 'freeze' while walking.


 OTHER CLINICAL FEATURES;

- GAIT: a typical short-shuffling or festinating gait is observed.This is because of the stooped posture and leads to a shorter stride length.It appears as if the patient is trying to avoid falling and is chasing his own centre of mass.Gait can be either anteropulsive(forward festinating) or retropulsive(backwadrs). Changing direction and turning is difficult so patient takes multiple small steps.Some patients stop only when there's an obstacle. Freezing episodes are way too common while walking.

- MOTOR PLANNING AND LEARNING:a typical 'start-hesitation' is seen.Carrying out complex movements is difficult.Micrographia or abnormally small and illegible handwriting is seen.Mask-like face is seen due to hypomimia or diminished expressiveness of face.Learning procedures is difficult but patient learns if the procedure is divided into steps which are commanded.

-SENSATIONS:sensory loss isn't seen but pain and parasthesias are common.Pain may also fluctuate according to the l-dopa administration.The pain increases in intensity while the patient is off the drug.In case of depression, the pain seems to increase too.Proprioceptive regulation may be affected making it difficult for the patient to judge the movements.Akathisia or an urge to move is commonly seen with restlessness.

 -SPEECH AND SWALLOWING: patient begins to sound monotonous and mutism may be seen in advanced cases.Dysphagia or difficulty in swallowing is common .

 -ANS:excessive sweating or seborrhea and excessive salivation or sialorrhea is seen.GI dysfunction,bladder dysfunction and sexual dysfunction is noted.

- CARDIOPULMONARY FUNCTION:orthostatic hypotension is common due to L-dopa. Respiratory impairments and airway obstruction are frequent.Kyphosis leads to reduced chest expansion and cardio pulmonary deconditioning.

- COGNITION AND BEHAVIOUR: depression , dysphoric mood and even dementia can be observed.Patients have troubles shifting attention.Slowness of thought and information processing is common.

Parkinson's Disease:etiology and pathophysiology

Parkinson's Disease (PD) - named after the discoverer James Parkinson.
Parkinson's Disease is a common chronic neuro-degenerative disease, characterised by rigidity,tremors,bradykinesia and postural instability.



Epidemiology:
It affects almost 2% of population within 50 -60 years of age.Men and women are affected equally.

Etiology:
1:Parkinson's disease is also known as 'paralysis agitants' and 'shaking palsy'
 It occurs due to damage to the substantia nigra and nigro strial pathway in the basal ganglia.
 It has two groups based on predominant features:
- Postural instability gait disturbed(PIGD) where the posture and gait are highly affected.
 -Tremor predominant, where tremors are a primary symptom.

2:Secondary parkinsonism: This includes the following types
-Post-infectious parkinsonism eg influenza epidemics of encephalitis lethargica.
-Toxic parkinsonism due to industrial poisons and chemicals like manganese, carbon disulfide,cyanide, methanol,etc.
-Drug induced Parkinsonism  due to drugs that interfere with dopaminergic mechanisms .For instance, chlorpromazine , haloperidol,amoxapine,methyldopa, reserpine. The effect of these drugs can be reversed as they only mimic the signs of PD.
-:Metabolic causes ,occurs in rare cases of metabolic conditions like hypothyroidism,hyperparathyroidism,hypoparathyroidism,wilson's disease.

3:Parkinson-plus syndromes :
 The parkinson-plus syndromes typically do not show improvement from the administration of anti-parkinson medication like levo-dopa.This is a differentiating factor between the two.
These are also neurodegenerative diseases that affect the substantia nigra and hence produce symptoms similar to PD.
These include:
-Striatonigral degeneration(SND) ,
-Progressive supranuclear palsy,
-Shy-Drager syndrome,
-Alzhimer's disease ,
-Wilson's disease,
-Diffuse lewy body disease, etc.

Pathophysiology
PD is associated with degeneration of neurons that produce Dopamine.
They have their cell bodies located in substantia nigra, of the basal ganglia.
The clinical features begin to appear with 30-60% degeneration of neurons.
To understand the pathophysiology of PD , we need to have a basic understanding  basal ganglia ,and its functions.


Basal ganglia (BG) is a collection of nuclear masses of grey matter deep within the brain.
It's made up of caudate and putamen together known as striatum.And also the globus pallidus, subthalamic nucleus,and substantia nigra.
BG  controlls the planning and programming of the movements by regulating the levels of kinetic activity , muscle tone and force.It translates thoughts into willed movements.
BG gets its input from the striatum from all the parts of cerebral cortex and substantia nigra.
Output is channelized by globus pallidus, substantia nigra to thalamus and back to cortex.

Direct pathway :here, the BG gives a direct output to thalamus and motor areas of cortex.
Indirect pathway :it suppresses some of the movements by not inhibiting the subthalamic nucleus.

Now, depletion of dopamine may result into the following:
-Overactive indirect pathway : which leads to akinesia and rigidity as it suppresses the movements.
-Underactive direct pathway: which leads to bradykinesia.
-Underactive indirect pathway: leads to hyperkinesia, chorea , hemiballismus.
-Overactive direct pathway : leads to dyskinesia,athetosis or dystonia.
-Loss of inhibition over BG explains tremors.

Spasticity

SPASTICITY


 INTRODUCTION:
 Spasticity is an abnormal increase in the tone of the muscle.It is a motor disorder characterised by hypertonia and velocity-dependent resistance to passive stretch.It is seen secondary to various disorders like stroke , cerebral palsy,etc.


 CHARACTERISTICS: 
Spasticity is velocity-dependent. So,the larger and quicker the stretch, the stronger is the resistance of the spastic muscle .It is seen only in one muscle group, either agonist or antagonist.
 During a rapid passive movement or stretch,initial high resistance or catch by the muscle , can be followed by a sudden letting-go or relaxation of the limb.This phenomena is called 'clasp-knife response'
 Spasticity is a state of 'hyperactivity' or exaggeration of the normal stretch reflex.
 It usually follows the Upper Motor Neuron lesions which include conditions like stroke, head -injury, cerebral palsy, multiple sclerosis,etc.
 The impairment of the following structures lead to spasticity- cerebral cortex, mid brain, brain stem, cerebellum and spinal cord.


 PATHOPHYSIOLOGY: The higher cortical centre (brain ) has an inhibitory control over the lower centres (skeletal muscles).
Spasticity arises from any injury to the higher cortical centre.
 Hence, there is an abnormality or inhibition of the 'supra-spinal' input . This leads to acute spasticity . Whereas, chronic spasticity may be associated with disability, abnormal posture and contracture formations.


 CLINICAL FEATURES:
 hyperactive stretch reflexes
 involuntary flexor and extensor spasms
 clonus
 babinski's sign 
exaggerated cutaneous reflexes
 dysseynergic patterns
 loss of precise autonomic control
 abnormal posture
 presence of primitive reflexes like ATNR, STNR ,TLR ,etc


 MANAGEMENT:
 1.POSITIONING:
 proper positioning of the limbs is necessary because chronic spasticity can be a result of improper positioning. 
Upper limbs should be placed in extension as they tend to adapt flexor synergy pattern.
 Lower limbs should be placed in slight flexion as they tend to adapt extensor synergy pattern. 
The neck should be neutral and supported.
 Various positioning interventions can be used, like prolonged positioning on a tilt-table, or low load weights applied using skin traction , etc. 


2.CRYOTHERAPY: Ice packs or wraps can be applied. Cool immersion bath (hydrotherapy) can be effective before starting the intervention.
 This temporarily reduces the spasticity by slowing the conduction of impulses in nerves and muscles. 
This is contra-indicated in patients with increased heart rate, respiratory rate and also nausea.


 3.SLOW SUSTAINED STRETCHING:
 Intermittant static stretch held for 30-60 seconds can be repeated 7-10 times per session.
 Maintained stretch for 30 minutes to 2 hours reduces stretch reflex activity.
 Stretch can be combined with gentle slow rhythmic rotation of the part.PNF techniques can also be used.
 A skeletal muscle relaxant like baclofen given during thee sessions is proved useful.


 4. ACTIVE EXERCISES:
 Should be performed slowly,at the available range only.
 Contraction of the antagonist, leads to reciprocal-inhibition of the agonist (spastic group) and helps to reduce spasticity.
 Mat exercises should be given.


 5.MYOFASCIAL RELEASE: it helps to reduce spasticity and induces relaxation.


 6.ELECTRICAL STIMULATION:This is given to the antagonistic group of muscles to decrease spasticity in agonists.


 7.LOWER TRUNK ROTATION: done in side lying or hook lying can reduce the extensor tone. 


8.BRACE OR SPLINTS : resting splints , toe/ finger spreader, ankle splint , etc are useful to maintain the positions of joints. 


9.OTHERS:
 Relaxed passive movements 
 Reflex inhibitory movement patterns
 Rood's approach


 Muscles prone to spasticity are Quadriceps, adductors and plantar flexors , so they should be given more attention.

Neurological Assessment

        The first step towards being a good physical therapist ,is to be able to assess the patient holistically .Let us begin with the assessment part.
NEUROLOGICAL ASSESSMENT

DEMOGRAPHIC DATA:this information helps the therapist to maintain records and communicate effectively with the patient .
NAME                                                                                                     ASSESSED BY
AGE                                                                                                        DATE
SEX
OCCUPATION
ADDRESS
WARD NO
BED NO
O.P.D NO
I.P.D NO
DATE OF ADMISSION

CHIEF COMPLAINT: This is the single most important complaint of the patient.
RELATIVE COMPLAINTS:These are related to chief complaint.A patient with only one complaint is a rare phenomena.

HISTORY OF PRESENT ILLNESS:This is a detailed explanation given by the patient,regarding the onset, time, duration,frequency, severity,etc. of the existing complaint.

PAST MEDICAL HISTORY: Only relevant history that relates to the existing complaint should be noted.For instance,history of hypertension in a CVA/ stroke patient.

PAST SURGICAL HISTORY: Relevant surgical history within the span of one decade can usually be considered important.For instance,any surgery over the face may cause facial palsy later ,due to injury to the  facial nerve.

DRUG HISTORY: To know if patient has been using some drugs for long term,for a condition.This sometimes can be of vital importance in case of stroke,which can be caused by unsupervised discontinuation of anti-hypertensives.

FAMILY HISTORY: Helps to know the prevalence of heriditory conditions in the family which could also be present in the patient.

PERSONAL HISTORY:
SLEEP: To know if the complaint disturbs patient's sleep.And helps to know patient's sleeping habits and sleep hygine.
APPETITE: To know if the appetite is reduced .
BOWEL/BLADDER: To know of existing incontinence , and hence, catheterization of the patient.
ADDICTIONS:Smoking, alcohol or other drugs abused by patients should be known.

SOCIAL AND ECONOMIC STATUS: It is important to know if the family is supportive or not , and if the patient can afford the treatment in case of long-term illness patients.

RELEVANT HISTORY:This is a skillfully drawn conclusion by the therapist, regarding the probable cause of the complaint , on basis of history alone.

GENERAL EXAMINATION: Physical therapy interventions are contra-indicated if the patient's vitals are very unstable or outside the normal range.
BLOOD PRESSURE : 
PULSE RATE :
RESPIRATORY RATE:
BODY TEMPERATURE:
ATTITUDE OF THE PATIENT:


SPECIFIC NEUROLOGICAL EXAMINATION:
HIGHER CORTICAL FUNCTIONS
CONSCIOUSNESS :Measured using Glasgow Coma Scale(GCS)
ORIENTATION : to time , place and person.
SPEECH: affected in conditions like Parkinsonism , Motor neuron disease, etc.
MEMORY:Recent and past memory tested to rule out amnesia.
VISION:can be impaired if optic nerve is affected.
HEARING: can be impaired if vestibulo-cochlear nerve is affected.for instance, tinnitus can be present.
UNDERSTANDING AND REASONING:absence of which leads to more dependence of the patient.

CRANIAL NERVE TESTING: all the 12 cranial nerves have to be tested.

MOTOR EXAMINATION:
TONE:Hypertonia/hypotonia should be noted . spasticity if present , can be measured using Modified Ashworth scale .
VOLUNTARY CONTROL: measured by vlountary control grade in case of upper motor neuron lesions
MUSCLE POWER: measured by manual muscle testing in case of lower motor neuron lesions.

REFLEXES: tested with a reflex hammer.They can be exaggerated, brisk , normal or diminished.
PLANTAR REFLEX/BABINSKI'S SIGN:
SUPERFICIAL REFLEXES:  abdominal reflex .
DEEP TENDON REFLEXES: biceps jerk, triceps jerk, bracioradialis , knee jerk,ankle jerk ,etc
PRIMITIVE /NEONATAL REFLEXES:Moro's reflex, ATNR,STNR,TLR,etc

BALANCE AND CO-ORDINATION
BALANCE:static and dynamic balance is tested using various tools like Romberg's sign , with eyes open ,closed and tandem walk position.
CO-ORDINATION TESTSfinger-finger, finger-nose, heel-shin, heel-toe, etc.

SENSATIONS: tested with patient in supine lying position and eyes preferably closed. best response is obtained when tested from distal to proximity.They can be present , absent or abnormal.
SUPERFICIAL SENSATIONS: fine touch, pain , temperature,tactile localozation , tactile discrimination.
DEEP SENSATIONS: crude touch,deep pressure, vibrations.
COMBINED CORTICAL SENSATIONS:kinaesthetic sensations, joint proprioception, stretch, stereognosis.

GAIT ASSESSMENT: make the patient walk independently if he/she can.abnormal gait patterns should be noted. step length, stride length,cadence step width, etc should be measured.

FUNCTIONAL ASSESSMENT: using Barthel index of FIM's score

PROVISIONAL DIAGNOSIS: this is 75% of diagnosis derived by the therapist on basis of above information and assessment.
DIFFERENTIAL DIAGNOSIS: these are other possible diagnoses which can be ruled out after investigations.

INVESTIGATIONS: MRI of the brain , CT scan of brain ,etc

DIAGNOSIS: this is the conclusive diagnosis of patient's existing problems.

ICIDH2 :
STRUCTURAL IMPAIRMENT:
FUNCTIONAL IMPAIRMENT:
ACTIVITY LIMITATIONS:
PARTICIPATION RESTRICTIONS:
POSITIVE CONTEXTUAL FACTORS:
NEGATIVE CONTEXTUAL FACTORS:


PROBLEM LIST OF PATIENT:

SHORT TERM GOALS:

LONG TERM GOALS:

MANAGEMENT:
AIMS: set up by the therapist which can be achieved by proper intervention
MEANS: to achieve the above aims.