Synonyms for hyporeflexia or Related words with hyporeflexia

areflexia              paresthesias              hypertonia              obtundation              dysesthesia              hypoesthesia              hyperarousal              anxiousness              anosmia              atonia              fasciculations              hypertonus              hemianesthesia              hypokinesia              hyperreflexia              hypotonia              hypoactivity              hemihypacusis              footdrop              presyncope              sleeplessness              akinesia              paraesthesia              hypesthesia              incoordination              ocularmotor              anosognosia              ataxic              dysgnosia              decerebrate              hemianopsia              pallor              hypervigilance              hemiparesis              osmophobia              derealization              dysarthria              tiredness              enervation              atonic              lightheadedness              dyskinetic              diaphoresis              hemianopia              giddiness              listlessness              hyperkinesia              dysmetria              hemihypesthesia              spasming             

Examples of "hyporeflexia"
Hyporeflexia may have other causes including hypothyroidism, electrolyte imbalance (including excess magnesium), drug induced (e.g. the symptoms of benzodiazepine intoxication include confusion, slurred speech, ataxia, drowsiness, dyspnea, and hyporeflexia).
Hyporeflexia is the condition of below normal or absent reflexes (areflexia). It can be tested for by using a reflex hammer. It is the opposite of a condition called hyperreflexia.
The symptoms of SSADH deficiency fall into three primary categories: neurological, psychiatric, and ocular. The most constant features seen are developmental delay, hypotonia and intellectual disability. Nearly half of patients seen manifest ataxia, behavior problems, seizures, and hyporeflexia.
Reports of overdose indicate that baclofen may cause symptoms including vomiting, weakness, sedation, somnolence, respiratory depression, seizures, unusual pupil size, dizziness, headaches, itching, hypothermia, bradycardia, hypertension, hyporeflexia, coma, and death.
Hyporeflexia is generally associated with a lower motor neuron deficit (at the alpha motor neurons from the spinal cord to muscle), whereas hyperreflexia is often attributed to upper motor neuron lesions (along the long motor tracts from the brain). The upper motor neurons are thought to be inhibitory of 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 lead to hyporeflexia and/or areflexia.
Rarely allergical reactions may occur (from dermal or mucosal symptoms to anaphylactic shock). At overdosing a toxical reaction arises - excitation, agitation, dishevelment, visual defects, buzzing in ears, muscle thrill to tremor, in more severe cases somnolence, hyporeflexia, breathing defects to apnea, convulsions.
The extensor Babinski reflex is usually absent. Muscle paresis/paralysis, hypotonia/atonia, and hyporeflexia/areflexia are usually seen immediately following an insult. Muscle wasting, fasciculations and fibrillations are typically signs of end-stage muscle denervation and are seen over a longer time period. Another feature is the segmentation of symptoms - only muscles innervated by the damaged nerves will be symptomatic.
CMV polyradiculomyelopathy (PRAM) is one of the five distinct neurological syndromes caused by CMV in HIV/AIDS. It causes subacute ascending lower extremity weakness with paresthesias and radicular pain, hyporeflexia or areflexia, and urinary retention. It has been suggested that CMV polyradiculomyelopathy should be treated with both ganciclovir and foscarnet in patients who develop the disease while taking either of these drugs.
Damage to upper motor neuron axons in the spinal cord results in a characteristic pattern of ipsilateral deficits. These include hyperreflexia, hypertonia and muscle weakness. Lower motor neuronal damage results in its own characteristic pattern of deficits. Rather than an entire side of deficits, there is a pattern relating to the myotome affected by the damage. Additionally, lower motor neurons are characterized by muscle weakness, hypotonia, hyporeflexia and muscle atrophy.
The strength of a reflex is used to gauge central and peripheral nervous system disorders, with the former resulting in hyperreflexia, or exaggerated reflexes, and the latter resulting in hyporeflexia or diminished reflexes. However, the strength of the stimulus used to extract the reflex also affects the magnitude of the reflex. Attempts have been made to determine the force required to elicit a reflex, but vary depending on the hammer used, and are difficult to quantify.
Mild hypokalemia is often without symptoms, although it may cause elevation of blood pressure, and can provoke the development of an abnormal heart rhythm. Severe hypokalemia, with serum potassium concentrations of 2.5–3 meq/l (Nl: 3.5–5.0 meq/l), may cause muscle weakness, myalgia, tremor, and muscle cramps (owing to disturbed function of skeletal muscle), and constipation (from disturbed function of smooth muscle). With more severe hypokalemia, flaccid paralysis and hyporeflexia may result. Reports exist of rhabdomyolysis occurring with profound hypokalemia with serum potassium levels less than 2 meq/l. Respiratory depression from severe impairment of skeletal muscle function is found in many patients.
Nemaline Myopathy is caused by mutations in one of at least 10 different genes. Nemaline myopathy is a clinically and genetically heterogeneous disorder and both autosomal dominant and autosomal recessive forms can occur. Diagnosis is made based upon clinical signs such as muscle weakness, absent or low deep tendon reflexes (hyporeflexia), and a high-arched palate, along with electron-dense aggregates, called nemaline rods, being observed at the microscopic level within muscle fibers. Genetic confirmation through identification of a known genetic mutation in the patient is also an important component of diagnosis.
A second form of neuroacanthocytosis, Levine-Critchley syndrome, was discovered by the American internist Irvine M. Levine in 1960 and reported in "Neurology" in 1964, and again in 1968. Subsequently, similar symptoms were identified and described by the British neurologist MacDonald Critchley in 1968. In both cases, the physicians described a hereditary syndrome that combined acanthocytosis with neurological peculiarities but normal serum lipoprotein. Specific symptoms included tics, grimacing, movement disorders, difficulty swallowing, poor coordination, hyporeflexia, chorea, and seizures. Patients often mutilated their tongues, lips, and cheeks. The diseases appeared in both sexes, and were usually diagnosed in infancy.
It is also used to counteract an overdose of Epsom Salts magnesium sulfate, which is often administered to pregnant women in order to prophylactically prevent seizures (as in a patient experiencing preeclampsia). Magnesium sulfate is no longer given to pregnant women who are experiencing premature labor in order to slow or stop their contractions (other tocolytics are now used instead due to better efficacy and side effect profiles). Excess magnesium sulfate results in magnesium sulfate toxicity, which results in both respiratory depression and a loss of deep tendon reflexes (hyporeflexia). Calcium gluconate is the antidote for magnesium sulfate toxicity.
Anterior spinal artery syndrome is necrosis of tissue in the anterior spinal artery or its branches. It is characterised by pain which radiates at onset and sudden quadraplegia (paralysis of all four limbs) or paraplegia (paralysis of the lower body). Within days, flaccid limbs become spastic and hyporeflexia (underactive nerve responses) turns into hyperreflexia (overactive nerve responses) and extensor plantar nerve responses. Sensory loss to pain and temperature also occurs up to the level of damage on the spinal cord, as damage to different areas will affect different parts of the body.
Succinic semialdehyde dehydrogenase deficiency (SSADHD), also known as 4-hydroxybutyric aciduria or gamma-hydroxybutyric aciduria, is a rare autosomal recessive disorder of the degradation pathway of the inhibitory neurotransmitter γ-aminobutyric acid, or GABA. The disorder has been identified in approximately 350 families, with a significant proportion being consanguineous families. The first case was identified in 1981 and published in a Dutch clinical chemistry journal that highlighted a person with a number of neurological conditions such as delayed intellectual, motor, speech, and language as the most common manifestations. Later cases reported in the early 1990s began to show that hypotonia, hyporeflexia, seizures, and a nonprogressive ataxia were frequent clinical features as well.
Spinal shock was first defined 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
Xylazine administration can lead to diabetes mellitus and hyperglycemia. Other possible side effects that can occur are areflexia, asthenia, ataxia, blurred vision, disorientation, dizziness, drowsiness, dysarthria, dysmetria, fainting, hyporeflexia, slurred speech, somnolence, staggering, coma, apnea, shallow breathing, sleepiness, premature ventricular contraction, tachycardia, miosis, and dry mouth. Rarely, hypotonia, dry mouth, urinary incontinence and nonspecific electrocardiographic ST segment changes occur. It has been reported that the duration of symptoms after human overdose is 8 to 72 hours. Further research is necessary to categorize the side effects that occur when xylazine is used in conjunction with heroin and cocaine.
Symptoms usually begin insidiously between adolescence and age 45. Syringomyelia develops in the center of the spinal cord, causing a central cord syndrome. Pain and temperature sensory deficits occur early but may not be recognized for years. The first abnormality recognized may be a painless burn or cut. Syringomyelia typically causes weakness, atrophy, and often fasciculations and hyporeflexia of the hands and arms; a deficit in pain and temperature sensation in a capelike distribution over the shoulders, arms and back is characteristic. Light touch and position and vibration sensation are not affected. Later, spastic leg weakness develops. Deficits may be asymmetric.
Signal intensity on a T2 image may be a result of edema or an inflammatory response. Because this type of imaging is a water detecting sequence, any form of calcification or mineralization would also appear dark, thus explaining why accumulation of extra blood or fluid would appear bright on a T2 image. Another explanation for signal intensity may be demyelination since the globus pallidi are traversed by a number of myelinated axons, thus confirming Ren and Mody’s 2003 work proving that repeated exposure of GHB to MAP kinase affected myelin expression, thus causing the numerous neurological dysfunctions seen in SSADH deficiency patients. Ultimately, because the globus pallidus is intimately linked with the basal ganglia and thalamus, it would be expected that some of the motor dysfunctions seen in SSADH patients such as ataxia and hyporeflexia would be common.