Motor neuron disease | Dr Anutosh Chakraborty

What is motor neuron disease (MND) ?

It is a progressive degenerative condition of unknown origin which attacks the cells of anterior horn of gray matter of the spinal cord, the motor nuclei of cranial nerves and corticospinal tracts. The most common age group to be affected is 30 to 60 years.

Types of MND

Five Types:

Amyotrophic lateral sclerosis (ALS) - This is the most well-known and traditional structure. A blended upper and lower engine neuron shortage is tracked down in the appendages. Side effects will quite often begin in the hands and feet with solid firmness as well as shortcoming from the start.

Progressive bulbar paralysis (PBP) - Bulbar contribution prevails inferable from sickness processes influencing essentially the engine cores of the cranial nerves. The bulbar muscles are impacted first, causing troubles in talking, biting and gulping.

Pseudobulbar Palsy (PsBP) - Bulbar contribution prevails in this assortment additionally, yet it is expected to reciprocal corticobulbar sickness and consequently reflects upper motor neuron brokenness.

Mixed progressive bulbar paralysis (PBP) - Mixed bulbar paralysis and pseudobulbar paralysis are structures that include the muscles of discourse and gulping. The nerves that control these capabilities are situated in the bulb (the lower part of the cerebrum), subsequently the term bulbar paralysis (loss of motion).

Primary lateral sclerosis-in which upper motor neuron harm brings about solidness and spastic loss of motion of the appendages. This is rare.

Cause of motor neuron disease

Motor neurons stimulate the muscles to move by passing on signals from the cerebrum. They assume a part in both cognizant and programmed developments, for example, gulping and relaxing.

Specialists trust that around 10% of MNDs are innate. The other 90% grow arbitrarily.

The specific causes are muddled, however the National Institute of Neurological Diseases and Stroke Trusted Source reports that hereditary, poisonous, viral, and other ecological variables might assume a part.

Symptoms / Signs

Usually onset is insidious and often begins with weakness and wasting of one or both hands, occasionally with spasticity and weakness in the legs.

Spinal muscular atrophy

• Difficult movement of fingers
• Later on it spreads to and may involve the anterior tibial and perineal muscles causing bilateral foot drop.
• Claw like deformity due to wasted, and hypothenar eminences.
• Weakness, wasting and fasciculations.
• Legs show weakness and spasticity.
• Reflexes exaggerated, superficial abdominal reflexes disappears.
• Spastic paraplegia in later stages develops.

Bulbar and pseudobulbar

• Fasciculations and weakness of tongue.
• Tongue looks small and wrinkled
• Speech slurred
• Dysphagia
• Regurgitation of food and liquids through nose
• Jaw jerk exaggerated 
• Dysarthria
• Impairment of emotional control

Upper motor neuron disease

A tremendous organization of nerve plots in the focal sensory system (CNS) which traverses the cerebral cortex, brain stem, cerebellum, and spinal line control the commencement and regulation of developments. The nerves in the CNS which convey the motivations for development are known as upper engine neurons (UMN). The essential plot which conveys signals for intentional development is known as the pyramidal parcel. The pyramidal plot isolates further into the corticospinal lot and the corticobulbar parcel. Injury or sores to UMN's are normal on account of the huge regions covered by the engine neuron pathways. UMN sores are assigned as any harm to the engine neurons that live above cores of cranial nerves or the foremost horn cells of the spinal rope. Harm to UMN's prompts a trademark set of clinical side effects known as the upper engine neuron condition. These side effects can incorporate shortcoming, spasticity, clonus, and hyperreflexia.

Lower motor neuron disease

A lower engine neuron sore is an injury which influences nerve filaments going from the lower engine neuron(s) in the foremost horn/front dark section of the spinal string, or in the engine cores of the cranial nerves, to the important muscle(s).[1]

One significant trademark used to distinguish a lower engine neuron injury is limp loss of motion - loss of motion joined by loss of muscle tone. This is as opposed to an upper engine neuron injury, which frequently gives spastic loss of motion - loss of motion joined by extreme hypertonia.

Radiology

MRI 

It utilizes strong magnets and radio waves to make pictures of designs inside your body. An MRI can show harm to upper motor neurons.

EMG, or electromyography. It involves a meager needle to check the movement in your muscles when they agreement and when they're very still. An EMG can check for issues with your lower engine neurons and assist with diagnosing ALS and PLS.

Another tests are:

Motor conduction testing

Muscle biopsy

Serum creative kinase level raised.

Differential diagnosis

• Syringo myelia
• Spinal tumor
• Diabetes mellitus, lead poisoning
• Cervical spondylosis
• Cervical rib
• Acute brachial neuritis
• Carpal; tunnel syndrome

Prognosis

Prognosis depends upon the sort of MND and the period of beginning. Some MNDs, like PLS or Kennedy's sickness, are not lethal and progress gradually. Individuals with SMA might seem, by all accounts, to be steady for extensive stretches, yet improvement ought not be normal. Some MNDs, like ALS and a few types of SMA, are lethal.

Treatment

Gastrostomy or cricopharyngeal myotomy if feeding via mouth or nasogastric tube becomes impossible.

Symptomatic treatment as required.

Physiotherapy

1) Active rehabilitation might assist with further developing posture, resists joint immobility, and slow muscle shortcoming and atrophy.

2) Extending and strengthening activities might assist with lessening spasticity, increment scope of movement, and keep course streaming.

Applying intensity might assuage muscle torment.

3) Assistive gadgets like backings or supports, orthotics, discourse synthesizers, and wheelchairs might assist certain individuals with holding independence. Hot compress may help for muscular pain to some extent.

4) Painless ventilation around evening time can resist apnea in rest, and a people may likewise require helped ventilation because of muscle shortcoming in the neck, throat, and chest during the daytime.

Homeopathic medicines for Motor neuron disease

Alumina :

Dizziness additionally that comes on while shutting the eyes, as is tracked down in spinal warm gestures, in sclerosis of back sidelong segments. Alum. It has delivered kind gestures comparable to crazy engine ataxia. It produces deadness of the bottoms of the feet, the fulgurating torments, the dizziness while shutting the eyes, and delivers faltering and aggravations of co-appointment.

Argentum Nitricum :

It has been utilized with stamped benefit in amyotrophic horizontal sclerosis. Boericke particularly referenced in this, there is spinal string degeneration, for example Sidelong Sclerosis.

Crotalus Horridus :

Easy loss of motion of the furthest points, with deadness and extraordinary briskness of impacted appendage. Numerous sclerosis, horizontal sclerosis, crazy engine ataxia moderate solid decay, lockjaw, Phatak says it has extraordinary impact in Sclerosis different, parallel. Moderate strong decay.

Curare:

Homeopathically it is in this manner fundamentally demonstrated in instances of loss of motion or moderate paresis like numerous sclerosis, amyotrophic parallel sclerosis, and so on. Tired torment all over spine. ARMS WEAK, HEAVY. Can't lift the fingers. Shortcoming of hands and fingers in piano players. Legs shake; give way in strolling. Weakness; loss of motion. Catalepsy. Favors advancement of corns. Reflexes decreased or abrogated.

Hypericum:

Torment in scruff of neck. Tension OVER SACRUM. Spinal blackout. Coccyx injury from fall, with torment transmitting up spine and down appendages. MOST IMPORTANT REMEDY FOR SPINAL INJURIES. Spinal Degeneration Lateral sclerosis Feeling of shortcoming and shudder of the relative multitude of appendages. Effect of weakness of the had arm and right foot. Can't stroll, from warmth of the spine.

Lathyrus sativus :

Pictures horizontal sclerosis and spastic paraplegic circumstances with unreasonably overstated reflexes. No aggravation, however, engine loss of motion of the lower the furthest points, nonappearance of decay. Extreme unbending nature of legs, spastic stride. Quivery, reeling stride. Knees thump together while strolling. Knee jerks overstated. Can't expand or cross legs while sitting. Sits bowed forward, fixes up with trouble. Solidness and weakness of the lower legs and knees. Heels don't contact the ground while strolling. Feet are hauled or put down abruptly and effectively while strolling. While resting, legs can be moved from one side to another yet can't be lifted. Legs blue, enlarged, if hanging down. Cramps in legs, more terrible cold and cold feet. Legs are cold during day, become hot and consume around evening time better revealing. Gluteal endlessly muscles of lower appendages are withered.

Plumbum Met :

Lead can cause a condition clinically undefined from engine neuron illness, especially one of its subtypes, amyotrophic parallel sclerosis (ALS). Lead in strength could presumably build the end of lead from the body, and subsequently may be valuable in conditions where de-calcification of bone prompts liberating of lead into the dissemination. It could hence be, at any rate, defensive in these conditions. It appears to be that the activity of lead on the sensory system is complicated, halfway including the myelin sheath of the nerves and mostly meddling in synaptic transmission. Generally, in traditional homeopathic writing, its utilization was suggested in epilepsy and engine deadens of the "wrist drop" type.

Cuprum Met :

It is valuable in AMYOTROPHIC, LATERAL, SPINAL SCLEROSIS and PARALYSIS of the cerebrum when there is regurgitating and fits with general briskness and blueness of the lips, subject to the retrocession of an intense ejection.

Amyotrophic sidelong spinal sclerosis; loss of motion after chorea circulatory trouble or typhoid and typhus; loss of motion of lower the furthest points after canker of psoas muscles; engine loss of motion with decay and compressions or choreic programmed developments, reasonableness typical; blockage in chest, palpitation of heart, beat slow, powerless and little; eyes shut, while opening them, eyeballs move about, eyelids jerk; frigid chilliness of feet or consuming in bottoms of feet; loss of motion climbing from fringe to focus.

Nux Vomica:

Amyotrophic parallel sclerosis. Spinal disturbance with unexpected loss of force in legs. Parallel spinal sclerosis. Spinal paleness. Myelitis and beginning phases of crazy engine ataxia.