Causes of Attention Deficit Hyperactivity Disorder
Attention Deficit Hyperactivity Disorder Causes: Book Excerpts
Attention Deficit Hyperactivity Disorder as a symptom:
Conditions listing Attention Deficit Hyperactivity Disorder
as a symptom may also be potential underlying causes of Attention Deficit Hyperactivity Disorder.
Our database lists the following as having
Attention Deficit Hyperactivity Disorder as a symptom of that condition:
Medications or substances causing Attention Deficit Hyperactivity Disorder:
The following drugs, medications, substances or toxins are some of the possible
causes of Attention Deficit Hyperactivity Disorder as a symptom.
This list is incomplete and various other drugs or substances
may cause your symptoms.
Always advise your doctor of any medications or treatments you are using,
including prescription, over-the-counter, supplements, herbal or alternative treatments.
Read more about medication causes of Attention Deficit Hyperactivity Disorder
What causes Attention Deficit Hyperactivity Disorder?
Article excerpts about the
causes of Attention Deficit Hyperactivity Disorder:
Attention Deficit Hyperactivity Disorder: NIMH (Excerpt)
Health professionals stress that since no one knows what causes ADHD,
it doesn't help parents to look backward to search for possible reasons.
There are too many possibilities to pin down the cause with certainty. It
is far more important for the family to move forward in finding ways to
get the right help.
Scientists, however, do need to study causes in an effort to identify
better ways to treat, and perhaps some day, prevent ADHD. They are finding
more and more evidence that ADHD does not stem from home environment, but
from biological causes. When you think about it, there is no clear
relationship between home life and ADHD. Not all children from unstable or
dysfunctional homes have ADHD. And not all children with ADHD come from
dysfunctional families. Knowing this can remove a huge burden of guilt
from parents who might blame themselves for their child's behavior.
Over the last decades, scientists have come up with possible theories
about what causes ADHD. Some of these theories have led to dead ends, some
to exciting new avenues of investigation.
One disappointing theory was that all attention disorders and learning
disabilities were caused by minor head injuries or undetectable damage to
the brain, perhaps from early infection or complications at birth. Based
on this theory, for many years both disorders were called "minimal
brain damage" or "minimal brain dysfunction." Although certain
types of head injury can explain some cases of attention disorder, the
theory was rejected because it could explain only a very small number of
cases. Not everyone with ADHD or LD has a history of head trauma or birth
complications.
Another theory was that refined sugar and food additives make children
hyperactive and inattentive. As a result, parents were encouraged to stop
serving children foods containing artificial flavorings, preservatives,
and sugars. However, this theory, too, came under question. In 1982, the
National Institutes of Health (NIH), the Federal agency responsible for
biomedical research, held a major scientific conference to discuss the
issue. After studying the data, the scientists concluded that the
restricted diet only seemed to help about 5 percent of children with ADHD,
mostly either young children or children with food allergies. (Source: excerpt from Attention Deficit Hyperactivity Disorder: NIMH)
Attention Deficit Hyperactivity Disorder: NIMH (Excerpt)
Drugs such as cocaine--including the smokable form known as crack--seem
to affect the normal development of brain receptors. These brain cell
parts help to transmit incoming signals from our skin, eyes, and ears, and
help control our responses to the environment. Current research suggests
that drug abuse may harm these receptors. Some scientists believe that
such damage may lead to ADHD.
Toxins in the environment may also disrupt brain development or brain
processes, which may lead to ADHD. Lead is one such possible toxin. It is
found in dust, soil, and flaking paint in areas where leaded gasoline and
paint were once used. It is also present in some water pipes. Some animal
studies suggest that children exposed to lead may develop symptoms
associated with ADHD, but only a few cases have actually been found.
(Source: excerpt from Attention Deficit Hyperactivity Disorder: NIMH)
Medical news summaries relating to Attention Deficit Hyperactivity Disorder:
The following medical news items are relevant to causes of Attention Deficit Hyperactivity Disorder:
Related information on causes of Attention Deficit Hyperactivity Disorder:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Attention Deficit Hyperactivity Disorder may be found in:
Causes of Attention Deficit Hyperactivity Disorder: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Attention Deficit Hyperactivity Disorder.
Agitation:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
❑ Alcohol withdrawal syndrome. Mild to severe agitation occurs in alcohol withdrawal syndrome, along with hyperactivity, tremors, and anxiety. With delirium, the potentially life-threatening stage of alcohol withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and a depressed mood. The patient’s pulse rate and temperature rise as withdrawal progresses; status epilepticus, cardiac exhaustion, and shock can occur.
❑ Anxiety. Anxiety produces varying degrees of agitation. The patient may be unaware of his anxiety or may complain of it without knowing its cause. Other findings include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache, back pain, insomnia, and tremors.
❑ Dementia. Mild to severe agitation can result from many common syndromes, such as Alzheimer’s and Huntington’s diseases. The patient may display a decrease in memory, attention span, problem-solving ability, and alertness. Hypoactivity, wandering behavior, hallucinations, aphasia, and insomnia may also occur.
❑ Drug withdrawal syndrome. Mild to severe agitation occurs in drug withdrawal syndrome. Related findings vary with the drug, but include anxiety, abdominal cramps, diaphoresis, and anorexia. With opioid or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated blood pressure, heart rate, and respiratory rate can also occur.
❑ Hepatic encephalopathy. Agitation occurs only with fulminating encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus, asterixis, and hyperreflexia.
❑ Hypersensitivity reaction. Moderate to severe agitation appears, possibly as the first sign of a reaction. Depending on the severity of the reaction, agitation may be accompanied by urticaria, pruritus, and facial and dependent edema.
With anaphylactic shock, a potentially life-threatening reaction, agitation occurs rapidly along with apprehension, urticaria or diffuse erythema, warm and moist skin, paresthesia, pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps, vomiting, and diarrhea can also occur.
❑ Hypoxemia. Beginning as restlessness, agitation rapidly worsens. The patient may be confused and have impaired judgment and motor coordination. He may also have tachycardia, tachypnea, dyspnea, and cyanosis.
❑ Increased intracranial pressure (ICP). Agitation usually precedes other early signs and symptoms, such as head-ache, nausea, and vomiting. Increased ICP produces respiratory changes, such as Cheyne-Stokes, cluster, ataxic, or apneustic breathing; sluggish, nonreactive, or unequal pupils; widening pulse pressure; tachycardia; a decreased LOC; seizures; and motor changes such as decerebrate or decorticate posture.
❑ Post-head trauma syndrome. Shortly after, or even years after injury, mild to severe agitation develops, characterized by disorientation, loss of concentration, angry outbursts, and emotional lability. Other findings include fatigue, wandering behavior, and poor judgment.
❑ Vitamin B6 deficiency. Agitation can range from mild to severe. Other effects include seizures, peripheral paresthesia, and dermatitis. Oculogyric crisis may also occur.
Other causes
❑ Drugs. Mild to moderate agitation, which is commonly dose related, develops as an adverse reaction to central nervous system stimulants — especially appetite suppressants, such as amphetamines and amphetamine-like drugs; sympathomimetics, such as ephedrine; caffeine; and theophylline.
❑ Radiographic contrast media. Reaction to the contrast medium injected during various diagnostic tests produces moderate to severe agitation along with other signs of hypersensitivity.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Deep tendon reflexes, hyperactive:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Amyotrophic lateral sclerosis (ALS)
ALS produces generalized hyperactive DTRs accompanied by weakness of the hands and forearms and spasticity of the legs. Eventually, the patient develops atrophy of the neck and tongue muscles, fasciculations, weakness of the legs and, possibly, bulbar signs (dysphagia, dysphonia, facial weakness, and dyspnea).
Brain tumor.
A cerebral tumor causes hyperactive DTRs on the side opposite the lesion. Associated signs and symptoms develop slowly and may include unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski's reflex.
Hypocalcemia
Hypocalcemia may produce a sudden or gradual onset of generalized hyperactive DTRs with paresthesia, muscle twitching and cramping, positive Chvostek's and Trousseau's signs, carpopedal spasm, and tetany.
Hypomagnesemia
Hypomagnesemia results in the gradual onset of generalized hyperactive DTRs accompanied by muscle cramps, hypotension, tachycardia, paresthesia, ataxia, tetany and, possibly, seizures.
Hypothermia
Mild hypothermia (90 to 94 F [32.2 to 34.4 C]) produces generalized hyperactive DTRs. Other signs and symptoms include shivering, fatigue, weakness, lethargy, slurred speech, ataxia, muscle stiffness, tachycardia, diuresis, bradypnea, hypotension, and cold, pale skin.
Preeclampsia.
Occurring in pregnancy of at least 20 weeks' gestation, preeclampsia may cause a gradual onset of generalized hyperactive DTRs. Accompanying signs and symptoms include increased blood pressure; abnormal weight gain; edema of the face, fingers, and abdomen after bed rest; albuminuria; oliguria; a severe headache; blurred or double vision; epigastric pain; nausea and vomiting; irritability; cyanosis; shortness of breath; and crackles. If preeclampsia progresses to eclampsia, the patient develops seizures.
Spinal cord lesion
Incomplete spinal cord lesions cause hyperactive DTRs below the level of the lesion. In a traumatic lesion, hyperactive DTRs follow resolution of spinal shock. In a neoplastic lesion, hyperactive DTRs gradually replace normal DTRs. Other signs and symptoms are paralysis and sensory loss below the level of the lesion, urine retention and overflow incontinence, and alternating constipation and diarrhea. A lesion above T6 may also produce autonomic hyperreflexia with diaphoresis and flushing above the level of the lesion, a headache, nasal congestion, nausea, increased blood pressure, and bradycardia.
Stroke.
A stroke that affects the origin of the corticospinal tracts causes the sudden onset of hyperactive DTRs on the side opposite the lesion. The patient may also have unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski's reflex.
Tetanus.
With tetanus, the sudden onset of generalized hyperactive DTRs accompanies tachycardia, diaphoresis, a low-grade fever, painful and involuntary muscle contractions, trismus (lockjaw), and risus sardonicus (a masklike grin).
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Attention deficit hyperactivity disorder:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
ADHD is thought to be a physiologic brain disorder with a familial tendency. Some studies indicate that it may result from disturbances in neurotransmitter levels in the brain due to reduced blood flow in the striated area of the brain. It affects 3% to 5% of school-age children and is three times more common in boys than in girls.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Agitation:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Affective disturbances
Agitation may occur in either the depressive or manic phase of affective disturbances and in personality disorders, such as borderline and antisocial personality disorders. The hallmark of the depressive form is depressed mood upon awakening, which eases during the day. Chronic anxiety may be mild or severe. Psychomotor agitation may be characterized by an inability to sit still, hand-wringing, pacing, and irritability. Other findings in the manic state may include decreased sleep, pressured speech, and grandiosity.
Alcohol withdrawal syndrome
Mild to severe agitation occurs with hyperactivity, tremors, and anxiety. In delirium tremens, the potentially life-threatening stage of alcohol withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and depressed mood. Pulse rate and temperature rise as withdrawal progresses; status epilepticus, cardiac arrhythmias, and shock can occur.
Anxiety
Anxiety is a common symptom that produces varying degrees of agitation. The patient may be unaware of his anxiety or may complain of it without knowing its cause. Other findings may include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache, back pain, insomnia, and tremors.
Chronic renal failure
Moderate to severe agitation occurs in chronic renal failure, which is marked by confusion and memory loss. The agitation is accompanied by diverse signs and symptoms, such as nausea, vomiting, anorexia, mouth ulcers, ammonia breath odor, GI bleeding, pallor, edema, dry skin, and uremic frost.
Dementia
Mild to severe agitation can result from many common dementia syndromes, such as Alzheimer’s and Huntington’s diseases. The patient may display a decrease in memory, attention span, problem-solving ability, and alertness. Hypoactivity, wandering behavior, hallucinations, aphasia, and insomnia may also occur.
Drug withdrawal syndrome
Findings vary with the drug but include mild to severe agitation, anxiety, abdominal cramps, diaphoresis, and anorexia. In opioid or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated blood pressure, heart rate, and respiratory rate can also occur.
Hepatic encephalopathy
Agitation occurs only in fulminating encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus, asterixis, and hyperreflexia.
Hypersensitivity reaction
Moderate to severe agitation may be the first sign of a hypersensitivity reaction. Depending on the severity of the reaction, agitation may be accompanied by urticaria, pruritus, and facial and dependent edema.
In anaphylactic shock, a potentially life-threatening reaction, agitation occurs rapidly along with apprehension, urticaria or diffuse erythema, warm and moist skin, paresthesia, pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps, vomiting, and diarrhea can also occur.
Hypoxemia
Beginning as restlessness, agitation rapidly worsens in hypoxemia. The patient may be confused and have impaired judgment and motor coordination. He may also have tachycardia, tachypnea, dyspnea, and cyanosis.
Increased intracranial pressure (ICP)
Agitation usually precedes other early signs and symptoms, such as headache, nausea, and vomiting. Increased ICP produces respiratory changes, such as Cheyne-Stokes, cluster, ataxic, or apneustic breathing; sluggish, nonreactive, or unequal pupils; widening pulse pressure; tachycardia; decreased LOC; seizures; and motor changes, such as decerebrate or decorticate posture.
Organic brain syndrome
In organic brain syndrome, agitation is manifested as hyperactivity, emotional lability, confusion, and memory loss. Slurred or incoherent speech and paranoid behavior may also occur.
Post–head trauma syndrome
Shortly—or even years—after injury, mild to severe agitation develops, characterized by disorientation, loss of concentration, angry outbursts, and emotional lability. Fatigue, wandering behavior, and poor judgment are other findings.
Vitamin B6 Deficiency
Agitation can range from mild to severe. Other effects include seizures, peripheral paresthesia, and dermatitis. Oculogyric crisis may also occur.
Other causes
Drugs
Mild to moderate agitation, which is commonly dose related, is an adverse effect of central nervous system stimulants—especially appetite suppressants, such as amphetamines and amphetamine-like drugs; sympathomimetics such as ephedrine; caffeine; and theophylline.
Radiographic contrast media
Injection of a contrast medium during various diagnostic tests may produce moderate to severe agitation along with other signs of hypersensitivity.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Deep tendon reflexes, hyperactive:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Amyotrophic lateral sclerosis
This disorder produces generalized hyperactive DTRs accompanied by weakness of the hands and forearms and spasticity of the legs. Eventually, the patient develops atrophy of the neck and tongue muscles, fasciculations, weakness of the legs and, possibly, bulbar signs (dysphagia, dysphonia, facial weakness, and dyspnea).
Brain tumor
A cerebral tumor causes hyperactive DTRs on the side opposite the lesion. Associated signs and symptoms develop slowly and may include unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski’s reflex.
Hepatic encephalopathy
Generalized hyperactive DTRs occur late and are accompanied by a positive Babinski’s reflex, fetor hepaticus, and a coma.
Hypocalcemia
This disorder may produce sudden or gradual onset of generalized hyperactive DTRs with paresthesia, muscle twitching and cramping, positive Chvostek’s and Trousseau’s signs, carpopedal spasm, and tetany.
Hypomagnesemia
This disorder results in gradual onset of generalized hyperactive DTRs accompanied by muscle cramps, hypotension, tachycardia, paresthesia, ataxia, tetany and, possibly, seizures.
Hypothermia
Mild hypothermia (90° to 94° F [32.2° to 34.4° C]) produces generalized hyperactive DTRs. Other signs and symptoms include shivering, fatigue, weakness, lethargy, slurred speech, ataxia, muscle stiffness, tachycardia, diuresis, bradypnea, hypotension, and cold, pale skin.
Multiple sclerosis
Typically, hyperactive DTRs are preceded by weakness and paresthesia in one or both arms or legs. Associated signs include clonus and a positive Babinski’s reflex. Passive flexion of the patient’s neck may cause a tingling sensation down his back. Later, ataxia, diplopia, vertigo, vomiting, urine retention, or urinary incontinence may occur.
Preeclampsia
Occurring in pregnancy of at least 20 weeks’ duration, preeclampsia may cause gradual onset of generalized hyperactive DTRs. Accompanying signs and symptoms include increased blood pressure; abnormal weight gain; edema of the face, fingers, and abdomen after bed rest; albuminuria; oliguria; severe headache; blurred or double vision; epigastric pain; nausea and vomiting; irritability; cyanosis; dyspnea; and crackles. If preeclampsia progresses to eclampsia, the patient develops seizures.
Spinal cord lesion
Incomplete spinal cord lesions cause hyperactive DTRs below the level of the lesion. In a traumatic lesion, hyperactive DTRs follow resolution of spinal shock. In a neoplastic lesion, hyperactive DTRs gradually replace normal DTRs. Other signs and symptoms are paralysis and sensory loss below the level of the lesion, urine retention and overflow incontinence, and alternating constipation and diarrhea. A lesion above T6 may also produce autonomic hyperreflexia with diaphoresis and flushing above the level of the lesion, headache, nasal congestion, nausea, increased blood pressure, and bradycardia.
Stroke
Any stroke that affects the origin of the corticospinal tracts causes sudden onset of hyperactive DTRs on the side opposite the lesion. The patient may also have unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski’s reflex.
Tetanus
In this disorder, sudden onset of generalized hyperactive DTRs accompanies tachycardia, diaphoresis, low-grade fever, painful and involuntary muscle contractions, trismus (lockjaw), and risus sardonicus (a masklike grin).
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Attention deficit hyperactivity disorder:
Causes
(Handbook of Diseases)
ADHD is commonly thought to be a physiologic brain disorder with a familial tendency. Some studies indicate that it may result from disturbances in neurotransmitter levels in the brain.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Agitation:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Affectivedisturbance
Agitation may occur in depressed and manic phases of affectivedisturbance and in personality disorders, such as borderline and antisocial personality disorders. In its depressive form, chronic anxiety occurs with varying severity. The hallmark is depressed mood upon awakening, which eases during the day. Psychomotor agitation may be characterized by an inability to sit still, hand-wringing, pacing, and irritability. Other findings in manic states may include decreased sleep, pressured speech, and grandiosity.
Alcohol withdrawal syndrome
With alcohol withdrawal syndrome, mild to severe agitation occurs. It may be accompanied by hyperactivity, tremors, and anxiety. With delirium tremens, the potentially life-threatening stage of alcohol withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and depressed mood. Pulse rate and temperature rise as withdrawal progresses; status epilepticus, cardiac exhaustion, and shock can occur.
Anxiety
Anxiety produces varying degrees of agitation. The patient may be unaware of his anxiety or may complain of it without knowing its cause. Other findings include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache, back pain, insomnia, and tremors.
Chronic renal failure
Moderate to severe agitation occurs with chronic renal failure, marked especially by confusion and memory loss. The agitation is accompanied by diverse signs and symptoms, such as nausea, vomiting, anorexia, mouth ulcers, ammonia breath odor, GI bleeding, pallor, edema, dry skin, and uremic frost.
Dementia
Mild to severe agitation related to dementia can result from many common syndromes, such as Alzheimer’s and Huntington’s diseases. The patient may display a decrease in memory, attention span, problem-solving ability, and alertness. Hypoactivity, wandering behavior, hallucinations, aphasia, and insomnia may also occur.
Drug withdrawal syndrome
In drug withdrawal syndrome, mild to severe agitation occurs. Related findings vary with the drug but include anxiety, abdominal cramps, diaphoresis, and anorexia. With narcotic or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated blood pressure, heart rate, and respiratory rate can also occur.
Hepatic encephalopathy
Agitation occurs with fulminating hepatic encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus (musty, sweet breath odor), asterixis, and hyperreflexia. Lethargy, aberrant behavior, and apraxia may also occur.
Hypersensitivity reaction
Moderate to severe agitation may be the first sign of a hypersensitivity reaction. Depending on the severity of the reaction, agitation may be accompanied by urticaria, pruritus, and facial and dependent edema.
With anaphylactic shock, a potentially life-threatening reaction, agitation occurs rapidly along with apprehension, urticaria or diffuse erythema, skin that’s warm and moist, paresthesia, pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps, vomiting, and diarrhea can also occur.
Hypoxemia
Beginning as restlessness, agitation rapidly worsens with hypoxemia. The patient may be confused and have impaired judgment and motor coordination. He may also have tachycardia, tachypnea, dyspnea, and cyanosis.
Increased intracranial pressure
With increased intracranial pressure (ICP), agitation usually precedes other early signs and symptoms, such as headache, nausea, and vomiting. ICP produces respiratory changes, such as Cheyne-Stokes, cluster, ataxic, or apneustic breathing; sluggish, nonreactive, or unequal pupils; widening pulse pressure; tachycardia; decreased LOC; seizures; and motor changes, such as decerebrate or decorticate posture.
Organic brain syndrome
With organic brain syndrome, agitation is manifested as hyperactivity, emotional lability, confusion, and memory loss. Slurred or incoherent speech and paranoid behavior may also occur.
Post–head trauma syndrome
Shortly after — or even years after — head trauma, mild to severe agitation develops, characterized by disorientation, loss of concentration, angry outbursts, and emotional lability. Other findings include fatigue, wandering behavior, and poor judgment.
Vitamin B6 deficiency
With vitamin B6 deficiency, agitation can range from mild to severe. Other effects include seizures, peripheral paresthesia, and dermatitis. Oculogyric crisis may also occur.
Other causes
Drugs
Mild to moderate agitation, which is commonly dose related, develops as an adverse reaction to central nervous system stimulants — especially appetite suppressants, such as amphetamines and amphetamine-like drugs; sympathomimetics such as ephedrine; caffeine; and theophylline.
Radiographic contrast media
Reaction to the contrast medium injected during various diagnostic tests produces moderate to severe agitation along with other signs of hypersensitivity.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Deep tendon reflexes, hyperactive:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS), which is also known as Lou Gehrig disease, produces generalized hyperactive DTRs accompanied by weakness of the hands and forearms and spasticity of the legs. Eventually, the patient develops atrophy of the neck and tongue muscles, fasciculations, weakness of the legs and, possibly, bulbar signs (dysphagia, dysphonia, facial weakness, and dyspnea).
Brain tumor
A cerebral brain tumor causes hyperactive DTRs on the side opposite the lesion. Associated signs and symptoms develop slowly and may include unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski’s reflex.
Hepatic encephalopathy
Generalized hyperactive DTRs occur late in the comatose stage of hepatic encephalopathy and are accompanied by a positive Babinski’s reflex, fetor hepaticus (a musty, sweet odor to the breath), and coma.
Hypocalcemia
Hypocalcemia may produce sudden or gradual onset of generalized hyperactive DTRs with paresthesia, muscle twitching and cramping, positive Chvostek’s and Trousseau’s signs, carpopedal spasm, and tetany. Other signs and symptoms include abdominal cramps, muscle cramps, arrhythmias, and diarrhea.
Hypomagnesemia
Hypomagnesemia results in gradual onset of generalized hyperactive DTRs accompanied by muscle cramps, hypotension, tachycardia, paresthesia, ataxia, tetany and, possibly, seizures. Other signs and symptoms include Chvostek’s sign, confusion, delusions, hallucinations, arrhythmias, and hypotension.
Hypothermia
Mild hypothermia (90°F to 94° F [32.2° C to 34.4° C]) produces generalized hyperactive DTRs. Other signs and symptoms include shivering, fatigue, weakness, lethargy, slurred speech, ataxia, muscle stiffness, tachycardia, diuresis, bradypnea, hypotension, and cold, pale skin.
Multiple sclerosis
Typically, hyperactive DTRs are preceded by weakness and paresthesia in one or both arms or legs in patients with multiple sclerosis. Associated signs include clonus and a positive Babinski’s reflex. Passive flexion of the patient’s neck may cause a tingling sensation down his back. Later, ataxia, diplopia, vertigo, vomiting, urine retention, or urinary incontinence may occur.
Preeclampsia
Occurring in pregnancy of at least 20 weeks’ duration, preeclampsia may cause gradual onset of generalized hyperactive DTRs. Accompanying signs and symptoms include increased blood pressure; abnormal weight gain; edema of the face, fingers, and abdomen after bed rest; albuminuria; oliguria; severe headache; blurred or double vision; epigastric pain; nausea and vomiting; irritability; cyanosis; shortness of breath; and crackles. If preeclampsia progresses to eclampsia, the patient develops seizures.
Spinal cord lesion
Incomplete spinal cord lesions cause hyperactive DTRs below the level of the lesion. In a traumatic lesion, hyperactive DTRs follow resolution of spinal shock. In a neoplastic lesion, hyperactive DTRs gradually replace normal DTRs. Other signs and symptoms of spinal cord lesion include paralysis and sensory loss below the level of the lesion, urine retention and overflow incontinence, and alternating constipation and diarrhea. A lesion above T6 may also produce autonomic hyperreflexia with diaphoresis and flushing above the level of the lesion, headache, nasal congestion, nausea, increased blood pressure, and bradycardia.
Stroke
Any stroke that affects the origin of the corticospinal tracts causes sudden onset of hyperactive DTRs on the side opposite the lesion. The patient may also have unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski’s reflex.
Tetanus
With tetanus, sudden onset of generalized hyperactive DTRs accompanies tachycardia, diaphoresis, low-grade fever, painful and involuntary muscle contractions, trismus (lockjaw), and risus sardonicus (a masklike grin).
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Agitation:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Alcohol withdrawal syndrome.Mild to severe agitation occurs in alcohol withdrawal syndrome, along with hyperactivity, tremors, and anxiety. With delirium, the potentially life-threatening stage of alcohol withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and a depressed mood. The patient's pulse rate and temperature rise as withdrawal progresses; status epilepticus, cardiac exhaustion, and shock can occur.
Anxiety.Anxiety produces varying degrees of agitation. The patient may be unaware of his anxiety or may complain of it without knowing its cause. Other findings include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache, back pain, insomnia, and tremors.
Dementia.Mild to severe agitation can result from many common syndromes, such as Alzheimer's and Huntington's diseases. The patient may display a decrease in memory, attention span, problem-solving ability, and alertness. Hypoactivity, wandering behavior, hallucinations, aphasia, and insomnia may also occur.
Drug withdrawal syndrome.Mild to severe agitation occurs in drug withdrawal syndrome. Related findings vary with the drug, but include anxiety, abdominal cramps, diaphoresis, and anorexia. With opioid or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated blood pressure, heart rate, and respiratory rate can also occur.
Hepatic encephalopathy.Agitation occurs only with fulminating hepatic encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus, asterixis, and hyperreflexia.
Hypersensitivity reaction.Moderate to severe agitation appears, possibly as the first sign of a reaction. Depending on the severity of the reaction, agitation may be accompanied by urticaria, pruritus, and facial and dependent edema.
With anaphylactic shock,a potentially life-threatening reaction, agitation occurs rapidly along with apprehension, urticaria or diffuse erythema, warm and moist skin, paresthesia, pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps, vomiting, and diarrhea can also occur.
Hypoxemia.Beginning as restlessness, agitation rapidly worsens. The patient may be confused and have impaired judgment and motor coordination. He may also have tachycardia, tachypnea, dyspnea, and cyanosis.
Increased intracranial pressure (ICP).Agitation usually precedes other early signs and symptoms, such as headache, nausea, and vomiting. Increased ICP produces respiratory changes, such as Cheyne-Stokes, cluster, ataxic, or apneustic breathing; sluggish, nonreactive, or unequal pupils; widening pulse pressure; tachycardia; a decreased LOC; seizures; and motor changes such as decerebrate or decorticate posture.
Post-head trauma syndrome.Shortly after, or even years after a head injury, mild to severe agitation may develop, characterized by disorientation, loss of concentration, angry outbursts, and emotional lability. Other findings include fatigue, wandering behavior, and poor judgment.
Vitamin B6 deficiency.Agitation can range from mild to severe. Other effects include seizures, peripheral paresthesia, and dermatitis. Oculogyric crisis may also occur.
Other causes
Drugs.Mild to moderate agitation, which is commonly dose related, develops as an adverse reaction to central nervous system stimulants—especially appetite suppressants, such as amphetamines and amphetamine-like drugs; sympathomimetics, such as ephedrine; caffeine; and theophylline.
Radiographic contrast media.Reaction to the contrast medium injected during various diagnostic tests produces moderate to severe agitation along with other signs of hypersensitivity.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Deep tendon reflexes, hyperactive:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Amyotrophic lateral sclerosis (ALS).ALS produces generalized hyperactive DTRs accompanied by weakness of the hands and forearms and spasticity of the legs. Eventually, the patient develops atrophy of the neck and tongue muscles, fasciculations, weakness of the legs and, possibly, bulbar signs (for example, dysphagia, dysphonia, facial weakness, and dyspnea).
Brain tumor.A cerebral tumor causes hyperactive DTRs on the side opposite the lesion. Associated signs and symptoms develop slowly and may include unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski's reflex.
Hypocalcemia.Hypocalcemia may produce a sudden or gradual onset of generalized hyperactive DTRs with paresthesia, muscle twitching and cramping, positive Chvostek's and Trousseau's signs, carpopedal spasm, and tetany.
Hypomagnesemia.Hypomagnesemia results in the gradual onset of generalized hyperactive DTRs accompanied by muscle cramps, hypotension, tachycardia, paresthesia, ataxia, tetany and, possibly, seizures.
Hypothermia.Mild hypothermia (90° to 94° F [32.2° to 34.4° C]) produces generalized hyperactive DTRs. Other signs and symptoms include shivering, fatigue, weakness, lethargy, slurred speech, ataxia, muscle stiffness, tachycardia, diuresis, bradypnea, hypotension, and cold, pale skin.
Preeclampsia.Occurring in pregnancy of at least 20 weeks' gestation, preeclampsia may cause a gradual onset of generalized hyperactive DTRs. Accompanying signs and symptoms include increased blood pressure; abnormal weight gain; edema of the face, fingers, and abdomen after bed rest; albuminuria; oliguria; a severe headache; blurred or double vision; epigastric pain; nausea and vomiting; irritability; cyanosis; shortness of breath; and crackles. If preeclampsia progresses to eclampsia, the patient develops seizures.
Spinal cord lesion.Incomplete spinal cord lesions cause hyperactive DTRs below the level of the lesion. In a traumatic lesion, hyperactive DTRs follow resolution of spinal shock. In a neoplastic lesion, hyperactive DTRs gradually replace normal DTRs. Other signs and symptoms are paralysis and sensory loss below the level of the lesion, urine retention and overflow incontinence, and alternating constipation and diarrhea. A lesion above T6 may also produce autonomic hyperreflexia with diaphoresis and flushing above the level of the lesion, a headache, nasal congestion, nausea, increased blood pressure, and bradycardia.
Stroke.A stroke that affects the origin of the corticospinal tracts causes the sudden onset of hyperactive DTRs on the side opposite the lesion. The patient may also have unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski's reflex.
Tetanus.With tetanus, the sudden onset of generalized hyperactive DTRs accompanies tachycardia, diaphoresis, a low-grade fever, painful and involuntary muscle contractions, trismus (lockjaw), and risus sardonicus (a masklike grin).
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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