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Hyporeflexia | |
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Other names | Hypo-reflexia, areflexia |
Specialty | Neurology |
Hyporeflexia is the reduction or absence of normal bodily reflexes. It can be detected through the use of a reflex hammer and is the opposite of hyperreflexia.[ citation needed ]
Hyporeflexia is generally associated with a deficit in the lower motor neurons (at the alpha motor neurons from the spinal cord to a muscle), whereas hyperreflexia is often attributed to lesions in the upper motor neurons (along the long, motor tracts from the brain). The upper motor neurons are thought to inhibit the reflex arc, which is formed by sensory neurons from intrafusal fibers of muscles, lower motor neurons (including alpha and gamma motor fibers) and appurtenant interneurons. Therefore, damage to lower motor neurons will subsequently result in hyporeflexia and/or areflexia.[ citation needed ]
In spinal shock, which is commonly seen in the transection of the spinal cord, hyporeflexia can transiently occur below the level of the lesion and can later become hyperreflexic. Cases of severe muscle atrophy or destruction may render the muscle too weak to show any reflex and should not be confused with a neuronal cause.[ citation needed ]
Hyporeflexia may have other causes, including hypothyroidism, electrolyte imbalance (e.g., excess magnesium), and drug use (e.g, depressants). [1]
Diseases associated with hyporeflexia include:
Lambert–Eaton myasthenic syndrome (LEMS) is a rare autoimmune disorder characterized by muscle weakness of the limbs. It is also known as myasthenic syndrome, Eaton–Lambert syndrome, and when related to cancer, carcinomatous myopathy.
Spasticity is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity, and hypertonia. It is also colloquially referred to as an unusual "tightness", stiffness, or "pull" of muscles.
A motor neuron is a neuron whose cell body is located in the motor cortex, brainstem or the spinal cord, and whose axon (fiber) projects to the spinal cord or outside of the spinal cord to directly or indirectly control effector organs, mainly muscles and glands. There are two types of motor neuron – upper motor neurons and lower motor neurons. Axons from upper motor neurons synapse onto interneurons in the spinal cord and occasionally directly onto lower motor neurons. The axons from the lower motor neurons are efferent nerve fibers that carry signals from the spinal cord to the effectors. Types of lower motor neurons are alpha motor neurons, beta motor neurons, and gamma motor neurons.
The ankle jerk reflex, also known as the Achilles reflex, occurs when the Achilles tendon is tapped while the foot is dorsiflexed. It is a type of stretch reflex that tests the function of the gastrocnemius muscle and the nerve that supplies it. A positive result would be the jerking of the foot towards its plantar surface. Being a deep tendon reflex, it is monosynaptic. It is also a stretch reflex. These are monosynaptic spinal segmental reflexes. When they are intact, integrity of the following is confirmed: cutaneous innervation, motor supply, and cortical input to the corresponding spinal segment.
The somatic nervous system (SNS), also known as voluntary nervous system, is a part of the peripheral nervous system (PNS) that links brain and spinal cord to skeletal muscles under conscious control, as well as to sensory receptors in the skin. The other part complementary to the somatic nervous system is the autonomic nervous system (ANS).
A reflex arc is a neural pathway that controls a reflex. In vertebrates, most sensory neurons do not pass directly into the brain, but synapse in the spinal cord. This allows for faster reflex actions to occur by activating spinal motor neurons without the delay of routing signals through the brain. The brain will receive the input while the reflex is being carried out and the analysis of the signal takes place after the reflex action.
The patellar reflex, also called the knee reflex or knee-jerk, is a stretch reflex which tests the L2, L3, and L4 segments of the spinal cord. Many animals, most significantly humans, have been seen to have the patellar reflex, including dogs, cats, horses, and other mammalian species.
Hyperreflexia is overactive or overresponsive bodily reflexes. Examples of this include twitching and spastic tendencies, which indicate disease of the upper motor neurons and the lessening or loss of control ordinarily exerted by higher brain centers of lower neural pathways.
An upper motor neuron lesion Is an injury or abnormality that occurs in the neural pathway above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves. Conversely, a lower motor neuron lesion affects nerve fibers traveling from the anterior horn of the spinal cord or the cranial motor nuclei to the relevant muscle(s).
Upper motor neurons (UMNs) is a term introduced by William Gowers in 1886. They are found in the cerebral cortex and brainstem and carry information down to activate interneurons and lower motor neurons, which in turn directly signal muscles to contract or relax. UMNs represent the major origin point for voluntary somatic movement.
Lower motor neurons (LMNs) are motor neurons located in either the anterior grey column, anterior nerve roots or the cranial nerve nuclei of the brainstem and cranial nerves with motor function. Many voluntary movements rely on spinal lower motor neurons, which innervate skeletal muscle fibers and act as a link between upper motor neurons and muscles. Cranial nerve lower motor neurons also control some voluntary movements of the eyes, face and tongue, and contribute to chewing, swallowing and vocalization. Damage to the lower motor neurons can lead to flaccid paralysis, absent deep tendon reflexes and muscle atrophy.
Spinal shock was first explored by Whytt in 1750 as a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transection. Reflexes in the spinal cord below the level of injury are depressed (hyporeflexia) or absent (areflexia), while those above the level of the injury remain unaffected. The 'shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock, which is life-threatening. The term "spinal shock" was introduced more than 150 years ago in an attempt to distinguish arterial hypotension due to a hemorrhagic source from arterial hypotension due to loss of sympathetic tone resulting from spinal cord injury. Whytt, however, may have discussed the same phenomenon a century earlier, although no descriptive term was assigned.
Pyramidal signs indicate that the pyramidal tract is affected at some point in its course. Pyramidal tract dysfunction can lead to various clinical presentations such as spasticity, weakness, slowing of rapid alternating movements, hyperreflexia, and a positive Babinski sign.
The vestibulospinal tract is a neural tract in the central nervous system. Specifically, it is a component of the extrapyramidal system and is classified as a component of the medial pathway. Like other descending motor pathways, the vestibulospinal fibers of the tract relay information from nuclei to motor neurons. The vestibular nuclei receive information through the vestibulocochlear nerve about changes in the orientation of the head. The nuclei relay motor commands through the vestibulospinal tract. The function of these motor commands is to alter muscle tone, extend, and change the position of the limbs and head with the goal of supporting posture and maintaining balance of the body and head.
The stretch reflex, or more accurately "muscle stretch reflex", is a muscle contraction in response to stretching a muscle. The function of the reflex is generally thought to be maintaining the muscle at a constant length but the response is often coordinated across multiple muscles and even joints. The older term deep tendon reflex is now criticized as misleading. Tendons have little to do with the response, and some muscles with stretch reflexes have no tendons. Rather, muscle spindles detect a stretch and convey the information to the central nervous system.
Alpha (α) motor neurons (also called alpha motoneurons), are large, multipolar lower motor neurons of the brainstem and spinal cord. They innervate extrafusal muscle fibers of skeletal muscle and are directly responsible for initiating their contraction. Alpha motor neurons are distinct from gamma motor neurons, which innervate intrafusal muscle fibers of muscle spindles.
The triceps reflex, a deep tendon reflex, is a reflex that elicits involuntary contraction of the triceps brachii muscle. It is sensed and transmitted by the radial nerve. The reflex is tested as part of the neurological examination to assess the sensory and motor pathways within the C7 and C8 spinal nerves.
A lower motor neuron lesion is a lesion which affects nerve fibers traveling from the lower motor neuron(s) in the anterior horn/anterior grey column of the spinal cord, or in the motor nuclei of the cranial nerves, to the relevant muscle(s).
The Golgi tendon reflex (also called inverse stretch reflex, autogenic inhibition, tendon reflex) is an inhibitory effect on the muscle resulting from the muscle tension stimulating Golgi tendon organs (GTO) of the muscle, and hence it is self-induced. The reflex arc is a negative feedback mechanism preventing too much tension on the muscle and tendon. When the tension is extreme, the inhibition can be so great it overcomes the excitatory effects on the muscle's alpha motoneurons causing the muscle to suddenly relax. This reflex is also called the inverse myotatic reflex, because it is the inverse of the stretch reflex.
Upper motor neuron syndrome (UMNS) is the motor control changes that can occur in skeletal muscle after an upper motor neuron lesion.