Diagnostic Tests for Paresthesia
Paresthesia Tests: Book Excerpts
Home Diagnostic Testing
These home medical tests may be relevant to Paresthesia:
- Diabetes: Related Home Testing:
- Nerve Neuropathy: Related Home Testing:
Paresthesia Diagnosis: Book Excerpts
Tests and diagnosis discussion for Paresthesia:
Diagnostic
evaluation is largely based on determining the underlying condition
causing the paresthetic sensations. An individual's medical history,
physical examination, and laboratory tests are essential for the
diagnosis. Physicians may order additional tests depending on the
suspected cause of the paresthesia.
(Source: excerpt from NINDS Paresthesia Information Page: NINDS)
Diagnostic Tests for Paresthesia: Online Medical Books
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PARESTHESIAS OF THE LOWER EXTREMITY:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The basic diagnostic workup includes a CBC, sedimentation rate, urinalysis, chemistry panel, arthritis panel, VDRL test, and x-ray of the lumbosacral spine. A serum B
12
and folic acid should be done if pernicious anemia is suspected. If these tests are negative, an orthopedic or neurologic specialist should be consulted. A CT scan of the lumbosacral spine, a nerve conduction velocity study, and an EMG may all be necessary in the workup. MRI is more expensive and often unnecessary.
Combined myelography and CT scan is often useful in evaluating the need for surgery. A bone scan may be helpful in diagnosing occult fractures, metastases, or osteomyelitis.
If multiple sclerosis, Guillain-Barré syndrome, or central nervous system lues are suspected, a spinal tap may be done. SSEP studies are useful in diagnosing multiple sclerosis.
A neuropathy workup may be necessary. This involves a glucose tolerance test to rule out diabetes; urine tests for porphyrins and porphobilinogen to rule out porphyria; quantitative urine niacin, thiamine, pyridoxine, and other B vitamins after loading, an ANA and anti-dsDNA test to rule out collagen disease; serum protein electrophoresis and immunoelectrophoresis to diagnose various collagen diseases and macroglobulinemia; a lymph node biopsy and Kveim test for sarcoidosis; nerve conduction velocity studies and EMG to establish the presence of a neuropathy; thyroid profile to rule out hypothyroidism or hyperthyroidism; HIV antibody titers; blood levels for heavy metals such as lead to rule out lead or arsenic neuropathy; and skin and muscle biopsies to rule out various collagen diseases. A trial of therapy is often necessary to rule out the nutritional neuropathies.
Lumbar puncture, as already mentioned, is useful in diagnosing Guillain-Barré syndrome. Nerve biopsy may be necessary when all the above procedures are negative.
RBC transketolase activity is decreased in beriberi and the serum pyruvate and lactate levels are elevated.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
PARESTHESIAS OF THE UPPER EXTREMITY:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
A CBC, sedimentation rate, urinalysis, chemistry panel, arthritis panel, and plain films of the cervical spine constitute the basic workup of paresthesias of the upper extremities. If these are negative, the next logical step is to consult a neurologist or neurosurgeon.
If there are paresthesias of the face or cranial nerve signs, MRI or CT scan of the brain will probably be the most logical test to order next. If not, MRI of the cervical spine will be useful. Nerve conduction velocity studies, EMG, and dermatomal SSEP studies complete the workup in most cases. However, SSEP studies and a spinal tap may be necessary to diagnose multiple sclerosis. If tabes dorsalis is suspected, a blood or spinal fluid fluorescent
Treponema pallidum
antibody test may be done. Immunoelectrophoresis may diagnose a monoclonal gammopathy.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
GAIT DISTURBANCES:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
Routine orders would include a CBC, sedimentation rate, chemistry panel, VDRL test, and urinalysis. If there is a painful limp, x-rays of the hip, knee, or ankle on the affected side should be performed. An x-ray of the lumbar spine will not usually be of great assistance, however. If plain x-rays are negative, a CT scan or MRI of the lumbar spine, hip, knee, or ankle may be of assistance in the diagnosis. A bone scan may pick up obscure fractures and other pathology.
If there are abnormalities on the neurologic examination, MRI or CT scan of the appropriate level of suspected pathology will be done. A spastic gait with abnormal cranial nerve findings would suggest a cerebral tumor or other brain disease, and a CT scan or MRI of the brain should be done. Keep in mind that the MRI is almost double the cost of a CT scan, and the diagnostic yield is not that much greater in many cases.
A spastic gait without cranial nerve signs or papilledema would suggest a spinal cord disorder, and an MRI or CT scan of the appropriate level of the spinal cord should be done. A CT scan of the cervical spine, however, is not very useful and MRI is preferred.
If multiple sclerosis is suspected, a spinal tap for myelin basic protein or gamma globulin levels should be done. A VEP study, a BSEP study, or a SSEP study will also be useful in diagnosing multiple sclerosis.
If there is an ataxic gait, cerebellar disorder should be suspected, and a CT scan of the brain may be done. However, an ataxic gait may also suggest multiple sclerosis, pernicious anemia, and tabes dorsalis. If the VDRL test is negative, a FTA-ABS test should be done. Blood levels for vitamin B
12
and folic acid will help diagnose pernicious anemia. A Schilling test, however, is sometimes necessary to facilitate this diagnosis. If muscular dystrophy is suspected, electromyographic examination and muscle biopsy will help confirm the diagnosis. If the patient has a steppage gait, the workup of peripheral neuropathy should be done, as noted on
page 350
.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Analgesia:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
After you’re satisfied that the patient’s spine and respiratory status are stabilized — or if the analgesia isn’t severe and isn’t accompanied by signs of spinal cord injury — perform a physical examination and baseline neurologic evaluation. First, take the patient’s vital signs and assess his level of consciousness. Then test pupillary, corneal, cough, and gag reflexes to rule out brain stem and cranial nerve involvement. If the patient is conscious, evaluate his speech, gag reflex, and ability to swallow.
If possible, observe the patient’s gait and posture and assess his balance and coordination. Evaluate muscle tone and strength in all extremities. Test for other sensory deficits over all dermatomes (individual skin segments innervated by a specific spinal nerve) by applying light tactile stimulation with a tongue depressor or cotton swab. Perform a more thorough check of pain sensitivity, if necessary, using a pin. (See Testing for analgesia, pages 38 and 39.) Also, test temperature sensation over all dermatomes, using two test tubes — one filled with hot water, the other with cold water. In each arm and leg, test vibration sense (using a tuning fork), proprioception, and superficial and deep tendon reflexes. Check for increased muscle tone by extending and flexing the patient’s elbows and knees as he tries to relax.
Focus your history taking on the onset of analgesia (sudden or gradual) and on any recent trauma — a fall, sports injury, or automobile accident. Obtain a complete medical history, noting especially any incidence of cancer in the patient or his family.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Skin, clammy:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If you detect clammy skin, remember that rapid evaluation and intervention are paramount. (See Clammy skin: A key finding, page 564.) Ask the patient if he has a history of type 1 diabetes mellitus or a cardiac disorder. Is he taking medications, especially an antiarrhythmic? Is he experiencing pain, chest pressure, nausea, or epigastric distress? Does he feel weak? Does he have a dry mouth? Does he have diarrhea or increased urination?
Next, examine the pupils for dilation. Also, check for abdominal distention and increased muscle tension.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Paresthesia:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
First, explore the paresthesia. When did abnormal sensations begin? Have the patient describe their character and distribution. Also, ask about associated signs and symptoms, such as sensory loss and paresis or paralysis. Next, take a medical history, including neurologic, cardiovascular, metabolic, renal, and chronic inflammatory disorders, such as arthritis or lupus. Has the patient recently sustained a traumatic injury or had surgery or an invasive procedure that may have damaged peripheral nerves?
Focus the physical examination on the patient’s neurologic status. Assess his level of consciousness (LOC) and cranial nerve function. Test muscle strength and deep tendon reflexes (DTRs) in limbs affected by paresthesia. Systematically evaluate light touch, pain, temperature, vibration, and position sensation. (See Testing for analgesia, pages 38 and 39.) Also, note skin color and temperature, and palpate pulses.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Analgesia:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Once you’re satisfied that the patient’s spine and respiratory status are stabilized—or if the analgesia isn’t severe and isn’t accompanied by signs of spinal cord injury—perform a physical examination and baseline neurologic evaluation. First, take the patient’s vital signs and assess his level of consciousness. Then test pupillary, corneal, cough, and gag reflexes to rule out brain stem and cranial nerve involvement. If the patient is conscious, evaluate his speech and ability to swallow.
If possible, observe the patient’s gait and posture and assess his balance and coordination. Evaluate muscle tone and strength in all extremities. Test for other sensory deficits over all dermatomes (individual skin segments innervated by a specific spinal nerve) by applying light tactile stimulation with a tongue depressor or cotton swab. Perform a more thorough check of pain sensitivity, if necessary, using a pin. (See Testing for analgesia, pages 48 and 49.) Also, test temperature sensation over all dermatomes, using two test tubes—one filled with hot water, the other with cold water. In each arm and leg, test vibration sense (using a tuning fork), proprioception, and superficial and deep tendon reflexes (DTRs). Check for increased muscle tone by extending and flexing the patient’s elbows and knees as he tries to relax.
Focus your history taking on the onset of analgesia (sudden or gradual) and on any recent trauma, such as a fall, a sports injury, or an automobile accident. Obtain a complete medical history, noting especially any incidence of cancer in the patient or his family.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Skin, clammy:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If you detect clammy skin, remember that rapid evaluation and intervention are paramount. (See Clammy skin: A key finding.) Ask the patient if he has a history of type 1 diabetes mellitus or a cardiac disorder. Is the patient taking any medications, especially an antiarrhythmic? Is he experiencing pain, chest pressure, nausea, or epigastric distress? Does he feel weak? Does he have a dry mouth? Does he have diarrhea or increased urination?
Next, examine the pupils for dilation. Check for abdominal distention and increased muscle tension.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Paresthesia:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
First, explore the paresthesia. When did the abnormal sensations begin? Have the patient describe their character and distribution. Ask about associated signs and symptoms, such as sensory loss and paresis or paralysis. Next, take a medical history, including neurologic, cardiovascular, metabolic, renal, and chronic inflammatory disorders, such as arthritis or lupus. Has the patient recently sustained a traumatic injury or had surgery or an invasive procedure that may have damaged peripheral nerves?
Focus the physical examination on the patient’s neurologic status. (See Differential diagnosis: Paresthesia, pages 602 and 603.) Assess his level of consciousness (LOC) and cranial nerve function. Test muscle strength and deep tendon reflexes (DTRs) in limbs affected by paresthesia. Systematically evaluate light touch, pain, temperature, vibration, and position sensation. (See Testing for analgesia, pages 48 and 49.) Note skin color and temperature, and palpate pulses.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Paresthesia and Dysesthesia:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. General examination. Perform a thorough examination and check for hypertension, tachypnea, and tachycardia.
B. Nervous system. Perform a sensory examination in the area of complaint: touch, pinprick, heat or cold, proprioception, and motor examination, including deep tendon reflexes.
1. Decreased sharp touch and thermal sensation suggest small fiber neuropathies (spinothalmic tract syringomyelia).
2. Decreased position sense, vibratory, or motor dysfunction but retention of most other cutaneous sensations are found with large fiber neuropathies.
3. Sometimes paresthesias alone do not suggest their origins, but when combined with other neurologic deficits, the cause becomes more clear.
4. Are the signs symmetrical? Do they occur in a graded fashion (polyneuropathy), somewhat asymmetric findings or multifocal signs (multiple mononeuropathy), or damaged individual cutaneous nerves?
C. Look for other physical signs of chronic disease such as alcoholism, diabetes, malnutrition, pulmonary disease, and acquired immunodeficiency syndrome.
D. Avoid testing a patient who is extremely fatigued (unreliable sensory examination). An overly cooperative patient may read too much into an examination and may discern very small differences that are not clinically significant. Do not prompt too much—give general directives.
Testing
(2–4)
A. Clinical laboratory tests that may be useful include complete blood count; liver, renal, and thyroid function tests; sedimentation rate; antinuclear antibodies; vitamin B12; and folate. Perform heavy metals and toxin assays if the history is suggestive.
B. The electromyelogram or nerve conduction study is the gold standard in assessing the origin of the neuropathy associated with the paresthesia, if indeed one exists. It can differentiate between axonal and demyelinating causes.
C. A nerve biopsy is most useful in suspected inflammatory disorders (vasculitis, amyloidosis). It is also useful in suspected, selected small-fiber neuropathies, and in undiagnosed chronic neuropathy where significant debilitation has occurred.
Diagnostic assessment
The positive phenomena of paresthesia and dysesthesia do not necessarily mean a devastating diagnosis. They can be troublesome with no clinical diagnosis or be harbingers of peripheral neuropathy. The negative phenomena usually are a more ominous sign. Positive phenomena can act as troublesome symptoms that have no clinical diagnosis or as harbingers of more complicated syndromes of the peripheral neuropathies. If there is a documented neurologic deficit, especially once the motor system becomes involved, then it is more imperative to make a diagnosis. The most frequent neuropathy seen in clinical practice is the diabetic neuropathy (5). The real emergent diagnosis is that of Guillian-Barré syndrome, in which paresthesia can rapidly progress to full motor loss within days. Important is the association of symptoms to true sensory or motor deficits, systemic illness, toxin or medication exposure, or the rapidity of worsening symptoms.
References
1. Asbury A. Numbness, tingling and sensory loss. In: Braunwald E, Fauci AS, Isselbacher DL, et al., ed. Harrison’s Principles of internal medicine, 14th ed. New York: McGraw-Hill, 1998:2457–2469.
2. Asbury AK, Thomas PK. Peripheral nerve disorders. Cambridge: Butterworth Heinemann, 1995:8.
3. Bradley W, Daroff R, Fenichel G, Marsden CD. Neurology in clinical practice, 2nd ed. Vols. I and II. Boston: Butterworth Heineman, 1996.
4. Haerer AF. The neurologic examination, 5th ed. Philadelphia: JB Lippincott, 1992.
5. Poncelet AN. An algorithm for the evaluation of peripheral neuropathy. Am Fam Physician 1998;57(4):755–760.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Visual Disturbance:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Homonymous hemianopsia may be perceived as blurring or as trouble finding the start of a line of print. On closer inspection, visual loss in corresponding fields in both eyes will be detected. This usually results from a lesion in the suprageniculate pathway. The macula is usually spared in cortical lesions. Bitemporal hemianopsia is due to a chiasmal lesion such as a pituitary adenoma, anterior communicating artery aneurysm, cerebellar tumor with third ventricle hydrocephalus, or meningitis. Thiamine deficiency, methanol toxicity, or optic neuritis at the chiasm can cause true acute bilateral visual loss
An afferent pupillary defect (Marcus Gunn pupil) is diagnostic for a prechiasmal optic nerve lesion. Have the patient fixate on a far object, and then shine a bright light into his or her eyes. The initial (abnormal) response is dilation instead of brisk contraction.
Tunnel vision causes a patient to turn his or her head to avoid bumping into objects, and it can be outlined by visual field confrontation. Causes include glaucoma, retinitis pigmentosa, and quinine toxicity.
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Source: Field Guide to Bedside Diagnosis, 2007
Skin, clammy:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Take vital signs and perform a cardiovascular assessment. Then proceed with the remainder of a complete physical assessment. Be sure to examine the pupils for dilation. Also, check for abdominal distention and increased muscle tension.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Paresthesia:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Focus the physical examination on the patient’s neurologic status. Assess his level of consciousness (LOC) and cranial nerve function. Test muscle strength and deep tendon reflexes (DTRs) in limbs affected by paresthesia. Systematically evaluate light touch, pain, temperature, vibration, and position sensation. Also, note skin color and temperature, and palpate pulses.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Vision Disturbances:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Goal ofprimary care physician is to detect any vision disturbance and torefer child to ophthalmologist for further evaluation and treatment.Normal visual acuity is estimated tobe 20/400 at birth. By 1 yr of age, acuity improves to 20/30as determined by sophisticated electrophysiologic and psychophysiologictechniques. By 2–3 yrs of age, some children have objectivevisual acuity of 20/40–20/50. 4-yr-oldscan usually read 20/30–20/40, whereas5-yr-olds should be reading 20/20–20/30.Any child with 2 or more lines of differencebetween the eyes should be suspected of having amblyopia. Neonates
Direct ophthalmoscope should be used to checkred reflex, which is reflection of light from retina. Color andintensity of reflex should be same in each eye. Mild eye misalignmentcan be normal finding at this age and usually disappears by 2 mosof age.
Infants
By 2–3mos, eyes of infants should be straight and they should be ableto follow large objects. At each visit red reflex should alwaysbe checked. Any difference in this reflex can indicate several eyeproblems, and ophthalmologic referral is mandatory.Corneal light reflex test can be usedto distinguish strabismus from pseudostrabismus. Reflection of lightsource (e.g., penlight or direct ophthalmoscope) should be in sameposition in each pupil. Normally, this reflection is just nasalof center of each pupil. If there is difference in its positionbetween 2 pupils, strabismus is present and referral is necessary. Preverbal Children
Exam forstrabismus is important at each well-child visit. In most instancesstrabismus occurs before 3 yrs of age.Esotropia (eye turning in) usuallyoccurs when child is looking at something near (e.g., picture ortoy), whereas exotropia (eye turning out) usually occurs when childis looking at object >10 ft away.Corneal light reflex and cover testscan be used to screen for these problems (see section on Strabismus). If ocularmisalignment is found, child should be referred to ophthalmologistfor further evaluation. Verbal Children
For children≥3 yrs of age, vision can be screened by several tests usingLea symbols, Tumbling E, the letters "HOTV", Snellennumbers or letters, and Allen recognition figures.Important to determine visual acuityof each eye and any difference in vision between the eyes, evenif it is just 1 line on chart.Child with vision of 20/40in both eyes or worse or difference of 2 lines in vision between theeyes should be referred for ophthalmologic evaluation.
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Alteration in Consciousness:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
When individualpresents with alteration of consciousness, diagnosis and treatment mustproceed concurrently, not serially.ABCs of resuscitation (airway, breathing,circulation) take precedence over other diagnostic and therapeuticmeasures. Airway must be cleared, and oxygen should be given bymask and bag ventilation.Failure of adequate ventilation requiresintubation.Hypotension or shock should be treatedwith volume expansion.With suspected or known head or necktrauma, head should be stabilized until lateral cervical spine radiographcan be performed to determine whether cervical spine injury hasoccurred.Level of consciousness and responsiveness,motor function, pupil size and responses, and extraocular movementsshould be evaluated. Presence or absence of meningeal signs as wellas focal hemispheric or brainstem findings also should be noted.Unless diagnosis has been establishedby history and physical exam, a number of tests need to be performed.Measurementof blood glucose should be done immediately at bedside.Blood should be sent for CBC with differential;serum electrolytes, glucose, creatinine, calcium, magnesium, ammonia;blood urea nitrogen; liver function tests; blood culture; and toxicology screen.Urine should be obtained for UA, urineculture, and toxicology screen. Vital Signs
Respiratory Rate and Pattern
Dyspneaand/or tachypnea may occur with pneumonia, any cause ofmetabolic acidosis, and lesions of lower midbrain–upperpontine tegmentum.Slow, irregular respirations may beassociated with drug intoxication, septicemia, and intracranialmass lesion. With acute head injury or diffuse brain damage of anycause, abnormal breathing patterns often overlap, making it difficultto relate specific pattern with discrete location of brain damage. Heart Rate
Bradycardia,if associated with hypertension and periodic breathing, suggestsincreased intracranial pressure.Tachycardia may occur with hypovolemicshock (dehydration, blood loss, diabetic ketoacidosis) and anticholinergicpoisoning. Blood Pressure
Hypertensionmay occur with increased intracranial pressure and with drug overdoses (amphetamines,cocaine, phencyclidine).Hypotension may occur with hypovolemia(fluid losses from gastroenteritis, acute blood loss, diabetic ketoacidosis),septicemia, adrenal insufficiency, and ingestion of alcohol or barbiturates. Temperature
Hyperpyrexiamay indicate presence of infection (bacterial meningitis, septicemia, pneumonia),heat stroke, or cocaine overdose. Although uncommon, brain lesionthat has disturbed temperature-regulating center also may producehyperpyrexia.Hypothermia may occur with severe hypovolemiaas well as with barbiturate or alcohol ingestion. Level of Consciousness and Responsiveness
Level ofconsciousness can be determined by noting degree of arousability.Response to name, simple commands,or painful stimuli (sternal pressure or pinching side of neck, innerarm, or thigh) can be used to evaluate degree of unresponsiveness.Eye opening or any form of speakingincluding grunting or groaning suggests some degree of functionof reticular activating system.Speech and purposeful withdrawal orlocalization of painful stimuli are signs of intact cortical function. Motor Function
Restlessmovements of arms and legs, variable resistance to passive movement,complex avoidance movements, and discrete protective movements generallyindicate intact corticospinal tracts, whereas asymmetry of functionmay indicate hemiparesis.Presence of posturing should be noted.Decorticate posturing consists of flexion of arms, wrists, and fingerswith adduction of upper extremities, and extension, internal rotation,and plantar flexion of lower extremities. Associated with diffusedamage to cerebral cortex and subcortical white matter or basalganglia. Decerebrate posturing, which consists of arm and hand extensionand back arching, is associated with extensive midbrain damage.Flaccid extremities and absence ofany motor response indicate further depression of brainstem function. Pupil Size and Responses
Exam ofpupils and their reactivity help determine level and location oflesions affecting reticular activating system in brainstem. Anyreactivity signifies intact parasympathetic and sympathetic pathwaysof oculomotor nerve. Bilateral lesions of midbrain that interruptthis pathway produce dilated unreactive pupils. Pontine lesionsproduce miotic pupils with only mild reaction to light. Unilateral pupillarydilatation suggests third nerve compression and impending uncalherniation.Generally, pupils remain reactive withmetabolic or toxic causes of coma. Exceptions include atropine orscopolamine poisoning, which causes dilated unreactive pupils; glutethimidepoisoning, which may cause medium to large unreactive pupils; opiatepoisoning (morphine, heroin), which causes pinpoint pupils withonly slight constriction to light; and severe anoxia with cardiacarrest, which produces fixed and dilated pupils. Miosis is usuallyseen with opiate, organophosphate, or clonidine overdosage, whereasmydriasis is usually seen with anticholinergic poisoning (tricyclicantidepressants) or with stimulant overdosage (amphetamines, cocaine). Extraocular Movements
Evaluationof eyes at rest, abnormal spontaneous eye movements, and ocularresponse to labyrinthine function provide important informationin assessment of alteration of consciousness.Cerebral lesions (usually frontal lobe)usually produce conjugate deviation of eyes to side of lesion andnormal labyrinthine responses, whereas unilateral pontine lesionsusually produce eye deviation away from side of lesion as well asabnormal labyrinthine responses. Midbrain lesions that involve oculomotornucleus or nerve or pontine lesions involving abducens nucleus ornerve may cause abduction of ipsilateral eye.Ocular response to vestibular stimulationalso helps evaluate integrity of brainstem function in childrenwith alteration of consciousness. Brainstem function is intact whenice water injection of 50 mL into external auditory canal with headflexed to 30 degrees produces conjugate horizontal eye deviationto side of injection and horizontal rapid nystagmus to oppositeside. Absence of such reflexes indicates severe brainstem dysfunction.Oculocephalic (doll's eye)reflex is also used to produce vestibular stimulation, but it iscontraindicated with suspected cervical spine injury. Head is rotatedfrom side to side and positive response indicating intact brainstemfunction is conjugate horizontal eye movement in opposite directionfrom head turn. Further Evaluation and Specific Diagnosis
Vital signsand assessments already described usually indicate whether any focal hemisphericor brainstem dysfunction exists. Final task is to make definitivediagnosis.Focal neurologic signs including asymmetricmovements and abnormal postures usually signify structural lesionin cerebral hemisphere, which also may affect brainstem function.Lesions above tentorium may cause alterationof consciousness by depression of large portions of both cerebralhemispheres, whereas lesions below tentorium (usually tumor or collectionof blood in posterior fossa) depress consciousness by compressionof brainstem structures.Presence of increased intracranialpressure may lead to central or uncal cerebral herniation. Centralherniation refers to rostrocaudal pattern of deterioration withloss of consciousness and irregular respirations followed by bilateraldilated unresponsive pupils and either decorticate or decerebrateposturing. Uncal herniation occurs more suddenly with loss of consciousnessand unilateral dilated pupil occurring almost simultaneously.Hemiparesis or hemiplegia may occurcontralateral to lesion.In cases of suspected structural lesion ± historyof head trauma, CT should be performed immediately. When herniationor impending herniation is suspected, patient should be intubated,hyperventilated, and given mannitol to acutely decrease increasedintracranial pressure prior to CT.Meningeal signs (stiff neck, Kernigor Brudzinski signs) commonly occur with bacterial meningitis andsubarachnoid hemorrhage. Lumbar puncture should be performed withsuspected bacterial meningitis or viral encephalitis. CT shouldbe performed first to rule out mass lesion in individuals with focalneurologic signs or symptoms of coma. If patient is unstable, appropriateantibiotic therapy should be given for suspected bacterial meningitisafter blood culture has been drawn, and lumbar puncture may be deferreduntil child is stable. In individuals with suspected subarachnoidhemorrhage and increased intracranial pressure, CT should be performedimmediately.Individuals without meningeal or focalneurologic signs may have head injury, drug intoxication, seizure,or metabolic disorder. Precise drug history is important but oftenis unavailable. 3 specific antidotes are available:Naloxone foropiate overdosePhysostigmine for anticholinergic poisoningFlumazenil for benzodiazepine overdose Metabolic causes of coma tend to producesymmetric hemispheric responses with normal brainstem function.With hyperammonemia in neonatal period,urea cycle defects and organic acid disorders should be suspected. Fig.3.1 (Adapted from Batshaw ML. Inborn errors of ureasynthesis. Ann Neurol 1994;35:137, with permission.) provides schemeto determine cause of hyperammonemia in neonates. Measurement ofserum ammonia, amino acids, lactate, and pyruvate, as well as urinaryorganic acids and orotic acid, will identify virtually all of geneticcauses of hyperammonia in this age group. Plasma acylcarnitine profilecan help diagnose various fatty acid oxidation defects. In a fewinstances (carbamyl phosphate synthetase and N-acetylglutamate synthetasedeficiencies), specific enzyme analysis must be performed to confirmdiagnosis. In infantsand children with hyperammonemia, scheme used for neonates can befollowed. However, if urinary organic acids are normal, prothrombintime and serum bilirubin should be measured. If these results areabnormal, liver disease, drugs, hepatotoxins, and Reye syndromeshould be considered. Also, if plasma citrulline is normal, plasmaarginine should be measured. Increase in plasma arginine signifiesarginase deficiency. Low or normal plasma arginine suggests 2 possibilities:lysine protein intolerance or hyperornithinemia-hyperammonemia-homocitrullinemiasyndrome. Increase in urinary lysine signifies lysine protein intolerance,whereas increase in plasma ornithine and urinary homocitrulline signifieshyperornithinemia-hyperammonemia-homocitrullinemia syndrome. Otherinvestigations depend on clinical findings and results of abovetests.
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Analgesia:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
After you're satisfied that the patient's spine and respiratory status are stabilized—or if the analgesia isn't severe and isn't accompanied by signs of spinal cord injury—perform a physical examination and baseline neurologic evaluation. First, take the patient's vital signs and assess his level of consciousness. Then test pupillary, corneal, cough, and gag reflexes to rule out brain stem and cranial nerve involvement. If the patient is conscious, evaluate his speech, gag reflex, and ability to swallow.
If possible, observe the patient's gait and posture and assess his balance and coordination. Evaluate muscle tone and strength in all extremities. Test for other sensory deficits over all dermatomes (individual skin segments innervated by a specific spinal nerve) by applying light tactile stimulation with a tongue depressor or cotton swab. Perform a more thorough check of pain sensitivity, if necessary, using a pin. (See Testing for analgesia, pages 32 and 33.)
Test temperature sensation over all dermatomes, using two test tubes—one filled with hot water, the other with cold water. In each arm and leg, test vibration sense (using a tuning fork), proprioception, and superficial and deep tendon reflexes. Check for increased muscle tone by extending and flexing the patient's elbows and knees as he tries to relax. Focus your history taking on the onset of analgesia (sudden or gradual) and on any recent trauma—a fall, sports injury, or automobile accident. Obtain a complete medical history, noting especially any incidence of cancer in the patient or his family. Obtain a complete drug history.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Skin, clammy:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If you detect clammy skin, remember that rapid evaluation and intervention are paramount. (See Clammy skin: A key finding, page 562.) Ask the patient if he has a history of type 1 diabetes mellitus or a cardiac disorder. Is he taking medications, especially an antiarrhythmic? Is he experiencing pain, chest pressure, nausea, or epigastric distress? Does he feel weak? Does he have a dry mouth? Does he have diarrhea or increased urination?
Next, take the patient's vital signs and pulse oximetry. Examine the pupils for dilation and check his level of consciousness. Note respiratory rate. Assess for respiratory distress. Auscultate the heart and lungs. Place the patient on a cardiac monitor and assess heart rhythm. Also, check for abdominal distention and increased muscle tension.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Paresthesia:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
First, explore the paresthesia. When did abnormal sensations begin? Have the patient describe their character and distribution. Also, ask about associated signs and symptoms, such as sensory loss and paresis or paralysis. Next, take a medical history, including neurologic, cardiovascular, metabolic, renal, and chronic inflammatory disorders, such as arthritis or lupus. Has the patient recently sustained a traumatic injury or had surgery or an invasive procedure that may have damaged peripheral nerves?
Focus the physical examination on the patient's neurologic status. Assess his level of consciousness (LOC) and cranial nerve function. Test muscle strength and deep tendon reflexes (DTRs) in limbs affected by paresthesia. Systematically evaluate light touch, pain, temperature, vibration, and position sensation. (See Testing for analgesia, pages 32 and 33.) Also, note skin color and temperature, and palpate pulses.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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