| Condition | Description | Cause | Manifestation | Treatment |
|---|---|---|---|---|
| Carpal Tunnel Syndrome | Compression-type focal neuropathy of median nerve | Bone dislocation, inflammation of tendons, pregnancy, diabetes mellitus | Pain, paresthesia and numbness of thumb and first 2 and 1/2 digits of hand, pain worse at night, atrophy of abductor pollicus | Avoid overuse, splinting, Anti-inflammatory drugs |
| Bell’s Palsy | Unilateral loss of facial nerve (CN 11) function | Linked to inflammatory reactions in or near the stylo-mastoid foramen, HSV-1, subluxation of TMJ or cervical vertebrae | Sudden onset of flaccid paralysis, unilateral, dry eyes, taste and speech affected, weak muscles on flaccid side | Combination of steroidal anti-inflammatories and anti-viral meds, massage, facial exercises |
| Trigeminal Neuralgia | Facial tics or grimaces characterized by stabbing pain along the unilateral sensory distribution of one or more of the trigeminal nerve branches | Idiopathic, mechanical pressure on nerve triggered by speaking, chewing, swallowing, sitting in a draft | Very painful, sharp, electric pain, 10-60 seconds of pain, muscular tic along pain path | Depends on source of pain, TMJ should be treated, acupuncture, analgesics |
| Multiple Sclerosis | Patchy demylenation of the CNS Classifications: Relapsing-Remitting: 1-2 flare ups every 1-3 years followed by remission Primary Progressive: after symptoms appear, deterioration occurs continuously without remissions Secondary Progressive: After years of relapse- remitting, it becomes continuous deterioration Progressive- Relapsing: steady progression from onset along with acute attacks | Autoimmune, exposure to common viruses, geography and genetics | Fatigue, optic signs, brain stem lesions, cognitive dysfunction, spinal cord lesions, paresthesia, pain | Corticosteroids, Beta interferons, physio |
| Alzheimer Disease | Progressive neurological disease that results in irreversible loss of nerve cells in the brain, leading to impaired memory, judgement, decision-making, concentration and language. Hallmarked by plaques and tangles | Unknown, Head injury, CAD, atherosclerosis | Stage 1: 2-4 years – short term memory loss, getting lost, changes in mood and behaviour, personality changes Stage 2: several years – difficulty performing familiar tasks, language problems, poor judgement, problems with abstract thinking Stage 3: 1-2 years – unable to recognize family and friends, apathetic, bed ridden | No cure, progressive disease, anti-oxidants, anti-inflammatories , cholinergic drugs, life long activity |
| Parkinson’s Disease | A degenerative disorder of motor functions characterized by involuntary tremors, progressive muscle rigidity, slowing of voluntary movements. Destruction of substantia nigra | Combination of genetic and environmental factors | Early : tremor at rest, unilateral, bradykinesia and akinesia, stiffness or rigidity, fatigue and depression Later: poor stability, sleep problems, dementia | L-DOPA, anticholinergics, Dopamine Agonists, physio |
| Seizures | Sudden, explosive and disorderly electrical active neurons which produces transit changes in brain function | In children: birth injury, hypoxia, infections, hypoglycaemia, genetics In adults: genetics, brain injury, stroke | ||
| Epilepsy | A condition of recurrent seizures that occur without an identifiable cause or cannot be corrected Classification: Partial Seizure : 1 hemisphere involved Simple – no loss of consciousness Complex – Impaired consciousness Secondarily Generalized – Begins as partial and progresses to Generalize Generalized Seizures: Initial involvement of both hemispheres Absence Seizure : zoning out Tonic- Clonic – Serious form Atonic- Sudden loss of muscle tone Myoclonic- Brief involuntary muscle contractions | Unknown | Partial : Facial movements, jerking of one part of body, tingling, sensory experiences of smells or sounds Generalized : Aura, unconsciousness, childhood absences, uncontrolled jerking, apnea, salivation, incontinence | Anticonvulsant drugs, surgery, vagus nerve stimulation |
Dylan Crake RMT & R.KIN 
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