Parkinson's Disease PDF

Parkinsonism (Parkinson Disease) PD  Dr/ Reham Ali Mohamed Ali Ahmed Lecturer of Neuromuscular disorders and its surgeries_ Faculty of physical therapy IN THE NAME OF ALLAH, THE MOST GRACIOUS, THE MOST MERCIFUL.  Origin: From area (6) and area (4) → descends to corp...

Parkinsonism (Parkinson Disease) PD  Dr/ Reham Ali Mohamed Ali Ahmed Lecturer of Neuromuscular disorders and its surgeries_ Faculty of physical therapy IN THE NAME OF ALLAH, THE MOST GRACIOUS, THE MOST MERCIFUL.  Origin: From area (6) and area (4) → descends to corpus striatum (part of basal ganglia) → Globus pallidus (part of basal ganglia) → from the globus pallidus fibers pass to; 1. Reticular formation 2. Vestibular nuclei 3. Red nucleus 4. Tectum of midbrain. From these nuclei the following extrapyramidal tracts arise: Motor areas 4 and 6 Corpus striatum B.G. Basal Ganglia Globus pallidus RF Vest. Nuclei Red Nucl. Tectum Ret.Spin T. Vest.Spin.T. Rubrospin. T. Tectospin. T.  1. Regulation and integration of voluntary motor. activity. Functions of the extrapyramidal 2. Regulation and maintenance of the system muscle tone. 3. Regulation and maintenance of emotional and associative movements.  Disturbance of the functions of the extra-pyramidal system leads to : 1) Disturbance in the integration and regulation of voluntary motor activity resulting in hyperkinesia i.e., STATIC TREMORS which may be of two main types: - Rhythmic and regular as in Parkinsonism. - Dysrhythmic and irregular as in chorea, athetosis and dystonia. N.B. : These tremors increase with emotional stress, anxiety and fatigue and disappear during sleep and during active voluntary movements. 2) Disturbance in the regulation and maintenance of normal muscle tone resulting in hypertonia described as RIGIDITY. 3) Disturbance in the regulation and maintenance of emotional and associated movements resulting in bradykinesia in the form of Mask Face, and loss of swinging during walking. Basal ganglia The basal ganglia (or basal nuclei) are a group of subcortical nuclei, of varied origin, in the brains , which are situated at the base of the forebrain and top of the midbrain.  The main components of the basal ganglia – as defined functionally – are: - the striatum; both dorsal striatum (caudate nucleus and putamen) and ventral striatum (nucleus - accumbens and olfactory tubercle), - globus pallidus, - ventral pallidum, - subthalamic nucleus, - and substantia nigra.   There are some differences in the basal ganglia. Basal ganglia are strongly interconnected with the cerebral cortex, thalamus, and brainstem, as well as several other brain areas. The basal ganglia are associated with a variety of functions, including control of voluntary motor movements, procedural learning, habit learning, eye movements, cognition, and emotion.  Substantia Nigra The substantia nigra (SN) is a basal ganglia structure located in the midbrain Substantia nigra is Latin for "black substance", reflecting the fact that parts of the substantia nigra appear darker than neighboring areas due to high levels of neuromelanin in dopaminergic neurons. consists of two parts with very different connections and functions: (the pars compacta (SNpc): input and the pars reticulata (SNpr): output) The substantia nigra is an important player in brain function, in particular, in: Eye movement, Motor planning, Motor learning, Reward-seeking, and Addiction. Dopamine NT Brain Reward System  Our brain has its own reward system. When we do certain things, the brain "rewards" us by making us feel good. The brain reward system is a brain circuit that causes feelings of pleasure when it's “turned on” by something we enjoy, like eating good food or being in love. Many people know dopamine as a pleasure or reward neurotransmitter. The brain releases dopamine during pleasurable activities Drugs activate the brain reward system in a similar manner. However, most drugs set off a surge of the brain chemical dopamine, so they produce a much stronger and longer-lasting “artificial” pleasure sensation than natural highs.  The effect of such a powerful reward strongly motivates people to take drugs again and again, even when they no longer really want to. That can happen because drugs can reprogram the brain, so that every time a person takes the drug, the effect is a little weaker. So, they have to take more and more of it to get the same feeling. Eventually, a person can become addicted to the drug and use it compulsively, not so much to feel good but to keep from feeling bad. That’s the “sneaky” part of addiction.  Parkinsonism Definition: Parkinson Disease is a chronic progressive neurological disease chiefly of later life that is linked to decreased dopamine production in the substantia nigra. Most people with parkinsonism have idiopathic Parkinson’s disease, also known as Parkinson’s. Idiopathic means the cause is unknown.  Parkinson's disease is a neurodegenerative disease characterized, in part, by the death of dopamine neurons in the SNpc.(substantia nigra pars compacta)  PARKINSONISM PATHOPHYSIOLOGY: It is due to deficiency of dopamine in the basal ganglia and substantia nigra. Basal ganglia (BG) controls movement Dopamine in BG inhibitory neurotransmitter Acetylcholine in BG excitatory neurotransmitter Without dopamine, inhibitory influences are lost So, neurons of BG are over stimulated, Excess muscle tone, tremors and rigidity are present. Causes:  Idiopathic(primary) parkinsonism vs symptomatic(secondary) parkinsonism Most patients (around 80-85 percent) diagnosed with Parkinson disease have what is called Primary parkinsonism or idiopathic Parkinson disease The remaining types of Parkinson when the cause of the disease is generally known are termed secondary or atypical parkinsonism or Parkinson Plus syndrome A.Idiopathic (Primary): Parkinson's disease (paralysis agitans). The cause is unknown. There is degeneration of the pigmented cells (neuromelanin) of the substantia nigra, which becomes pale. The basal ganglia are also affected. This degeneration leads to deficiency of dopamine in the brain. The age of onset is above 50 years. Both sexes are equally affected. B.Symptomatic (Secondary): There is a known cause which leads to deficiency of dopamine in the brain, but without structural changes in the substantia nigra or basal ganglia. Inflammatory: Encephalitis. Vascular: Cerebral atherosclerosis. Toxic. Neoplastic: Tumors of the basal ganglia. Traumatic: Repeated trauma to the head as in boxers.  :The commonest causes of Parkinsonism are 1) Paralysis agitans. 2) Post-encephalitis. 3) Atherosclerosis Type acc to Paralysis Post-encephalitic Atherosclerosis cause agitans  Age 40-60 years Any age Over 60 years Onset Gradual Usually, acute Gradual Course Progressive Regressive or Remissions & stationary Relapse Tremors Tremors more Rigidity & tremors Rigidity more than &rigidity than rigidity equally marked tremors Clinical Features of Parkinson Disease a) Cardinal symptoms : b) Secondary motor manifestation c) Non-motor manifestation d)Other clinical manifestations may be found in some cases (mainly postencephalitic) a) Cardinal symptoms Tremors T Rigidity R Slowness of movement (bradykinesia)/ Akinesia - kinesia A paradoxica) Postural Instability P  PD Symptoms AC.CH Dopamine Tremor Rigidity bradykinesia Loss of associated reaction Decrease postural reaction tremor Regular, rhythmic oscillatory movement (pill-rolling) The most common symptom unilateral, typically resting tremor in body parts, most commonly in the upper extremities It is an early symptom and is seen in about 70% of people presenting with Parkinson. Related to an imbalance of neurotransmitters, dopamine and acetylcholine They increase with emotional stress and fatigue and disappear during sleep and voluntary movements.  Rigidity Involuntary increase in the muscle tone present throughout the range of movement Hypertonia in form of rigidity Lead-pipe cog-wheel  Rigidity - It may be present throughout the act (ROM) to the same degree & is then described as lead pipe rigidity; it may be interrupted by the tremors & is then described as cog wheel rigidity. - Affecting the proximal more than the distal muscles. - Affecting more the flexors of the neck, trunk, limbs resulting in the gorilla-like attitude. - Causing difficulty in starting the act of walking leading to a slow, shuffling (festinant or short steppage) gait with propulsion. - Prolonged rigidity results in contractures and postural deformity Typical appearance of parkinsonian patient Bradykinesia Bradykinesia can be the most disabling symptom of the condition and refers to slowness, decreased movement amplitude, and dysrhythmia. However Immobile patients who become excited may be able to make quick movements such as catching a ball (or may be able to suddenly run if someone screams "fire"). This phenomenon (kinesia paradoxica) suggests that patients with PD have intact motor programs but have difficulties accessing them without an external trigger, such as a loud noise, marching music or a visual cue requiring them to step over an obstacle. Postural instability Postural instability is one of the most disabling features of PD. Postural instability is often experienced in the late stages of PD and is a marker of disease progression. (Righting – Equilibrium – Protective)  b) Secondary motor manifestation Freezing Micrographia Loss of emotional and associative movements : resulting in: - Immobile face, with frequent blinking -Mask-like expression (Hypomimia ) - Monotonous speech. - Loss of swinging of the arms during walking. Unwanted accelerations Fatigue Difficulty rolling in bed or rising from a seated position. Impaired fine motor dexterity and motor coordination. Impaired gross motor coordination. Akathisia: an unpleasant desire to move Speech and swallowing disturbance Hypophonia Monotonic Drooling Dysphagia Freezing An important sign of Parkinson disease is freezing of gait, when patients temporarily feel as if their feet are glued to the floor and hesitate before stepping forward. After the first step, people usually resume their normal stride. Micrographia Micrographia refers to the shrinkage in Parkinson patients’ handwriting. This happens as a result of bradykinesia, which causes difficulty with repetitive actions. Gait and posture disturbances : Slow gait Decreased arm-swing Short step Turning "en bloc": Stooped forward-flexed posture Shuffling gait + Gait freezing Festination c) Non-motor manifestation Pain, Anosmia, anxiety, constipation, depression, and problems with memory and sleep disturbance - (The pars compacta also plays a role in temporal processing and is activated during time reproduction) - Pain: if there is affection in subthalamus nucleus D) Other clinical manifestations may be found in some cases (mainly postencephalitic): Oculo-gyric crisis: sudden spasm of the conjugate movement of the eyes, mainly upwards. Mental problems: e.g., depression (hidden symptoms)-Obesity Impotence or amenorrhea Prognosis: ▪ Slowly progressive ▪ Long subclinical period of around 5 years ▪ 61% die within 10 years and 83% die within 15 years ▪ Mean survival with L-dopa ▪ Mortality is due to cardiovascular diseases or pneumonia Diagnosis of Parkinson disease: Clinical Rating Scales Unified Parkinson disease rating scale, the Hoehn and Yahr staging scale, Schwab and England functional assessment scale and a set of validated tests.  The UPD rating scale is the most used scale in the clinical study of Parkinson disease. The current UPDRS includes four subscales. Subscale 1 covers mentation, behavior, and mood. Subscale 2 rates activities of daily living. Subscale 3 is a clinician rating of the motor manifestations of PD. Subscale 4 covers complications of therapy. Data for subscales 1, 2, and 4 are elicited from patients and caregivers, whereas data for subscale 3 is examination-based.  Rigidity assessment acc. to UPDRS 0 Normal No rigidity. 1 Slight  Rigidity only detected with activation maneuver. 2 Mild Rigidity detected without the activation maneuver, but full range of motion is easily achieved. 3 Moderate Rigidity detected without the activation maneuver; full range of motion is achieved with effort. 4 Sever Rigidity detected without the activation maneuver and full range of motion not achieved.  Yahr Classification Of Disability Of Parkinsonism Stages Character of disability I Minimal or absent, Unilateral if present II Minimal bilateral or Midline involvement. Balance not impaired III Impaired righting reflexes unsteadiness when turning or rising from chair. Some activities are restricted, but patient can live independently and continue to work IV All symptoms present and severe. Requires help with. some activities of daily living. V Confined to bed or wheelchair unless aided Medical treatment : Levo—Dopa Levo-Dopa + Carbi-Dopa Dopamine agonists. Anticholinergic drugs. Amantadine hvdrochloride  Parkinsonism (Parkinson Disease) PD Parkinson Assess & Rehab  Assessment HISTORY General Examination: Mental Examination Speech Examination Oro-Facial Examination Motor System Examination  Motor Assessment in Parkinsonism by Inspection: 1. Involuntary movements (tremors) 2. Skeletal deformities 3. Patient’s posture (flexion attitude) 1. Involuntary movements (Tremors) 0= No tremor. 1= Tremor is mild, writing and drawing spiral minimally impaired, no disability in feeding or dressing. 2= Tremor is moderate, writing and drawing spiral impaired, mild to moderate difficulty with feeding and dressing 3= Tremor is marked, writing and drawing spiral illegible, marked impairment of feeding and dressing. 4= Tremor is severe, writing and drawing cannot be performed, unable to feed or dress 2.Skeletal deformities  Motor assessment by Palpation Examination of muscle tone (rigidity) Muscle strength examination A- group muscle testing B- functional muscle testing Examination of postural reactions Balance examination Examination Of Reflexes Joint Rom Examination Sensation - Pain Examination – Co-ordination Examination Gait Examination Functional Examination Examination Of Bradykinesia  Examination of Muscles Tone & REFLEXES Hypertonia Hyporeflexia (They may be normal or difficult to elicit due the presence of rigidity. Deep reflexes are hyporeflexia).  MANAGEMAENT 1- Orofacial Dysfunction 2- Rigidity 3- Bradykinesia 4- Tremors Strategy: 5-Cardiopulmonary training strategies: 6- Restless leg syndrome: 7-Balance and Postural problems & prevention of falls strategy: 8- Gait training strategies: 9- EMG Biofeedback 10- Icing and other topical anesthetic 11- Group Therapy. 12-Serial casting, splinting techniques 13- Transcranial magnetic stimulation 14-Surgical interventions for parkinsonism 1- Orofacial dysfunction A- Deep breathing exercises Diaphragmatic breathing Pursed lip breathing Segmental breathing (costal expansion) Apical breathing Lateral costal expansion Posterior basal expansion Spiro meter B-PNF for the head and neck to strength the facial muscles C-Treating Mask Face : Facial exercise : Raise your eyebrows and wrinkle your forehead. Open your mouth widely as you can -Try to whistle Blow out your cheeks -wiggle your nose.  2- RIGIDITY Relaxation technique PNF Rotatory exercises and extension exe Sensory reinforcement Increase movement awareness.  3-BRADYKINESIA To help patient to overcome bradykinesia (get to sit from supine on bed)=turn complex task to simple sub-tasks First, It is a complex sequential motor skill that has many subcomponents, which include: 1. Throwing back the bed covers 2. Shifting the pelvis toward the center of the bed so that, when the turn is completed, the body is not too the edge 3. Turning the head 4. Bringing the arm across the body in the direction of rolling 5. Swinging the legs over the edge, 6. Pushing up 7. Adjusting postural alignment to sit upright  4- Tremor Tremors can be controlled by several methods: a. By immobilization using a rigid brace across a joint fixing it in one position b. Weighting involves the addition of weight to a part of the body Limb weights: Tremor-suppressing orthoses 5-Cardiopulmonary training strategies Breathing ex. / PNF with UL movement improve trunk extension – daily walking. 6- Restless leg syndrome walking – stretching – massage – hot or cold bath – relaxation techniques. 7-Balance and Postural problems & prevention of falls strategy A- Flexibility exercises B- Strengthening exercises C- PNF patterns D-Positioning E- Postural correction F- visual feedback training using biodex balance system 8- Gait training strategies A) Physical Therapy to improve Gait B) Treadmill training C) External cues D) U turn training pattern E) Task specific training  9- EMG Biofeedback The clinical application of biofeedback to improve a patient's motor control begins by re- educating by providing visual or audio feedback of electromyogram (EMG), positional or force parameters in real time. 10- Icing and other topical anesthetic Limb cooling Cooling induced tremor reduction 11- Functional activities Overcome Falling by: 12- Depression Treated by family accompany the patient in walking, traveling and group therapy. 13- Role of family Give his family information:Explain to relative anatomy and physiology of the disease will help to understand and improve psychological state. Teach family type of exes to do at home. Use videotape or computer for feedback. Patient and family should accept fluctuation in ADL performance like aging which is a fact of life. Celebrity Disease World Parkinson's Day Thank you