Amyotrophic lateral sclerosis (ALS)

The diagnosis of amyotrophic lateral sclerosis (ALS) is primarily clinical. When the disease has progressed far in its course and involves many parts of the body, the patient’s appearance and the findings on the neurologic examination may provide sufficient evidence for the diagnosis. When a patient presents with the first symptoms, however, making the diagnosis is not straightforward.[19]
ALS may be suspected whenever an individual develops insidious loss of function or gradual, slowly progressive, painless weakness in 1 or more regions of the body, without changes in the ability to feel, and no other cause is immediately evident.
In lower motor neuron (LMN) involvement, fasciculations may occur early on in the disease, particularly in the tongue and limbs. Patients with upper motor neuron (UMN) involvement generally are hyperreflexic and stiff. Reflexes may be diminished due to LMN involvement. UMN symptoms may include spasms and sudden, uncontrolled straightening movements of the lower limbs.
In 75-80% of patients, symptoms begin with limb involvement, while 20-25% of patients present with bulbar symptoms. For those with limb involvement at presentation, the frequency of upper limb versus lower limb involvement is approximately equal.
Patients with upper limb onset have twice the likelihood for onset in the dominant arm, compared with the nondominant arm. There is equal likelihood for presentation in either lower extremity. Women have a greater frequency of bulbar (speech dysfunction) onset than men. These observations suggest a greater likelihood for network dismantling to start where there is a better-developed, or more complex, cortical network.
Patients who have lower limb onset initially may complain of tripping, stumbling, or awkwardness when running. Foot drop is common, and patients may report a 'slapping' gait.
Persons with upper limb onset may experience reduced finger dexterity, cramping, stiffness, and weakness or wasting of intrinsic hand muscles. This may lead to difficulty with actions such as buttoning clothes, picking up small objects, or turning a key. These patients may develop wrist drop.
As ALS progresses, muscle atrophy becomes more apparent, and spasticity may compromise gait and manual dexterity. Immobility, if coupled with spasticity, may lead to the development of painful joint contractures. Muscle cramps are common. In some patients, persistent stiffness or cramping of muscles may stress the related joints and the back. This can usually be ameliorated with medications and physical therapy exercises to relax the muscles and maintain joint range of motion.
Bulbar involvement
A mixture of spastic and flaccid components may characterize speech, resulting in a dysarthria with severe disintegration and slowness of articulation. Hypernasality occurs from palatal weakness, and patients may develop a strained, strangled vocal quality. With time, speech may be lost, and patients may become dependent on other forms of communication, such as writing, communication boards, or speech-generation devices.
Patients with bulbar involvement may develop swallowing difficulties (dysphagia). Swallowing liquids requires the greatest oropharyngeal muscle control; therefore, patients usually report more difficulty with liquids than with solids. Aspiration or choking during a meal may occur.
Drooling affects some patients and results from a combination of excessive salivation, poor swallowing, and poor lip control. The problem can usually be ameliorated effectively with oral medications or a scopolamine patch, but other methods, such as salivary gland irradiation or injection of botulinum toxin, are sometimes required.
Pseudobulbar symptoms
These consist of exaggerated, involuntary emotional responses. The response may be of one type (laughter or crying) or, less commonly, alterations in emotive expressions. Episodes of intense laughter may be followed immediately by tears. The patient's response often does not correspond to an apparent social stimulus or the current psychosocial situation; it may instead be an exaggerated response to a minor trigger. The patient is aware of the lack of control. Symptoms can often be ameliorated by medications.
Preserved functions
Certain motor neurons usually are spared in ALS, which means that some functions are preserved. Most patients retain extraocular movements and bowel and bladder control. With progressive disease, patients may develop problems with urge incontinence and constipation because of weak abdominal musculature, but sphincter control generally is unaffected.
Since the disease primarily involves motor neurons, sensory function typically is preserved, although a minority of patients complains of some numbness and paresthesias. Abnormalities have been reported on sensory nerve conduction studies in a small number of patients with ALS,[155] but these findings often reflect the presence of an unrelated, coexistent condition.
Skin integrity in ALS usually is maintained, primarily due to the combination of preserved sensory function and continued control of bowel and bladder function. Some studies of patients with ALS have found morphologic changes in the skin that are complex and poorly understood but that may contribute to preservation of skin integrity.
Family history
Obtaining a thorough family history is pertinent in the examination of all patients. Patients with a family history of Mendelian ALS may be considered to have definite ALS as soon as any evidence of motor neuron disease arises that cannot be accounted for by an alternative explanation, regardless of the extent of involvement. Some experts, however, require that the abnormal gene be demonstrated in the patient. Genetic testing is typically recommended when a mode of inheritance, most often autosomal dominant, is recognized, but the gene has not yet been identified in the family.
A family history in a second- or third-degree relative or a family history of frontotemporal dementia should also be regarded as strong evidence in support of a diagnosis of familial ALS

Lathyrus sativus pictures lateral sclerosis and spastic paraplegic conditions with excessively exaggerated reflexes. No pain, but motor paralysis of the lower extremities, absence of atrophy. Excessive rigidity of legs, spastic gait. Tremulous, tottering gait. Knees knock together when walking. Knee jerks exaggerated. Cannot extend or cross legs when sitting. Sits bent forward, straightens up with difficulty. Stiffness and lameness of the ankles and knees. Heels do not touch the ground when walking. Feet are dragged or put down suddenly and forcibly while walking. While lying down legs can be moved from side to side but cannot be lifted. Legs blue, swollen, if hanging down. Cramps in legs, worse cold and cold feet. Legs are cold during day, become hot and burn at night better uncovering. Gluteal muscles and muscles of lower limbs are emaciated.

Plumbum Met :
lead can cause a syndrome clinically indistinguishable from motor neuron disease, particularly one of its subtypes, amyotrophic lateral sclerosis (ALS). Lead in potency could probably increase the elimination of lead from the body and therefore might be useful in conditions where decalcification of bone leads to freeing of lead into the circulation. It might therefore be, at least, protective in these circumstances. It seems that the action of lead on the nervous system is complex, partly involving the myelin sheath of the nerves and partly interfering in synaptic transmission. Traditionally, in classical homoeopathic literature, its use was recommended in epilepsy and motor paralyses of the 'wrist drop' type.



Cuprum Met :
It is useful in AMYOTROPHIC, LATERAL, SPINAL SCLEROSIS and PARALYSIS of the brain when there is vomiting and spasms with general coldness and blueness of the lips, dependent upon the retrocession of an acute eruption.
Amyotrophic lateral spinal sclerosis; paralysis after chorea apoplexy or typhoid and typhus; paralysis of lower extremities after abscess of psoas muscles; motory paralysis with atrophy and contractions or choreic automatic movements, sensibility normal; congestion in chest, palpitation of heart, pulse slow, weak and small; eyes closed, when opening them, eyeballs move about, eyelids twitch; icy coldness of feet or burning in soles of feet; paralysis ascendens from periphery to centre.

Nuxvomica:
Amyotropic lateral sclerosis .Spinal irritation with sudden loss of power in legs. Lateral spinal sclerosis. Spinal anemia. Myelitis and early stages of locomotor ataxia.


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Dr.Deoshlok Sharma
[message edited by deoshlok on Thu, 21 Aug 2014 04:10:54 BST]