Anatomy and Physiology of neuron and supporting structures

Neurons, are the primary cells found in the nervous system. They are similar to other cells as
they have a cell body called soma. The nucleus is situated in the soma. Neurons produce several
proteins which could execute their functions. These proteins are mostly synthesized in soma (2).

Another important anatomical structure is dendrite which extends from the cell body in the form
of appendages. Dendrites are short and branching processes. They extend into axon which is
longer than the dendrites (2). All the neurons are capable of three important functions. These
include:

1. Receiving signals or information

2. Integrating the incoming information and deciding if the information shall be carried to
the effector organs
3. Communication through signals to target other cells such as neurons, muscles or glands.

Supporting structures:

Glial cells help neurons and are responsible for sustaining their environments. Oligodendrocytes,
astrocytes, ependymal cells, and microglial cells support the neurons and are found in the central
nervous system (2). Surrounding axons, oligodendrocytes are responsible for creating the myelin
sheath. Astrocytes feed neurons, regulate their extracellular environment, and sustain them
structurally.

Propagation of an action potential:

When a neuron transfers information down the axon away from the cell body, it creates an action
potential. Through one point on the cellular membranes, the action potential occurs. It spreads
along the membranes, depolarizing the next section of the tissue in a progressive manner (8). As
a result, an action potential constantly travels from the neuronal core to the tissue via the axon.

Question 2:

ALS causes nerve cell loss in the major parts of brain such as brainstem and the motor nucleus.
Although the precise cause underpinning specific motor neuron deterioration is unknown,
evidence suggests that oxidation, apoptosis, irregular neurofilament feature, faults in synaptic
transmission, misfolded proteins preparation and deterioration, increased inflammation, and
mitochondrial malfunction are all possible contributors (1). Since ALS solely impairs the motor
processes, it has little effect on the cognitive or autonomic processes.

Peripheral neuropathy is characterised by weakness, tingling, and discomfort in the feet and
hands as a result of trauma to nerves situated beyond the brainstem. Traumatic injuries,
infections, metabolism issues, hereditary factors, and toxic exposure can all induce peripheral
neuropathy (3). Nerve tissue injury can result from vascular and circulatory issues that reduce
oxygen delivery to the peripheral nerves. Neuropathy can be caused by diabetic, tobacco, and
artery narrowing high blood pressure and atherosclerosis (fatty plaques on the interior of blood
vessels). Vasculitis can induce arterial wall thickening and fibrosis, obstructing blood flow and
causing patchwork nerve injury, known as mononeuropathy multiplex in which individual nerves
in various regions are affected.

Fractures can cause nerve damage by putting pressure on surrounding nerves, and displaced discs
between vertebra can pinch nerve fibres as they arise from the spinal column. Arthritis, extended
strain on a nerve (such as from a cast), or continuous, violent activities can expand ligaments and
tendons, narrowing slender neural channels. Carpal tunnel syndrome and ulnar neuropathy are
two frequent kinds of neuropathy caused by trapped or pinched nerves near the wrist and elbow
respectively (4). 

Question 3:

Weight loss with ALS is a common problem. It develops not just in combination with dysphagia,
but also because of illness-specific factors not yet completely understood. The weight loss in
ALS is explained by greater energy loss via muscle twitching, increased respiratory work,
hypermetabolism and a reduced consumption of food as a result of depression (5). In either case,
weight loss and a decreased body-mass-index (BMI) are widely recognised to be adverse
predictors of ALS longevity.

Considering the heterogeneous aetiology of ALS, knowing changes in the muscle fiber
mechanism may assist to communicate the significance of faulty cell function to motor neuron
pathology. Muscular metabolism defines the main portion of the entire body cell function and the
fibre type and strength as well as length of muscle training form a heterogeneous composition
and adaptation of the muscle tissue mechanism (6).

ALS patients usually lose significant muscle mass since their muscles are atrophied by disuse
and since they can effectively ingest adequate nutrients to sustain bodyweight. The patients with
ALS are often dependent on tube feeding which has been significantly associated with weight
loss.

The weight loss in ALS is mainly due to dysphagia development, but could not be always linked
to dysphagia. The reduction of weight had a detrimental influence on standard of living and was
related to shorter lifespan (7). Weight loss can also occur following to nonspecific weariness,
low hunger and related depression in people often with bulbar dysfunction. Malnourishment is a
poor reduction in appetite and a high degree of metabolism can also lead to weight loss.
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