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Diagnostic Tests 

Diagnostic Tests
Chapter:
Diagnostic Tests
Author(s):

Andrea C. Adams

DOI:
10.1093/med/9780190206895.003.0002
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date: 29 October 2020

The diagnostic tests used most often to evaluate patients who have disease of the central nervous system (CNS) include cerebrospinal fluid (CSF) analysis, electroencephalography (EEG), evoked potentials, electromyography (EMG), computed tomography (CT), and magnetic resonance imaging (MRI). These tests should be used to supplement or to extend the clinical examination. Remember that diagnostic tests have technical limitations and the quality of the results depends on the examiner or laboratory performing the test. The results should always be interpreted in the context of the patient’s clinical presentation.

CSF Analysis and Lumbar Puncture

CSF is usually obtained by lumbar puncture. Before performing this straightforward but invasive procedure, know its indications and contraindications. Laboratory evaluation of CSF is indicated for the diagnosis and treatment of intracerebral hemorrhage and infectious, neoplastic, and demyelinating diseases of the CNS. With increasing knowledge about degenerative disorders, prions, and other neurologic problems, CSF analysis may become more useful.

Lumbar puncture should not be performed in patients with a known or suspected intracranial or spinal mass because of the potential for herniation and neurologic compromise with a shift in intracranial pressure. In these patients, CT or MRI is recommended before lumbar puncture is performed. However, neuroimaging should not delay the diagnosis or treatment of suspected meningitis. The risk of missing the diagnosis of meningitis is much greater than the risk of herniation. In this life-threatening illness, empiric treatment with antibiotics may need to be started to avoid delay in therapy (see Chapter 13). Clinical indications that lumbar puncture can be performed safely are nonfocal findings on neurologic examination and the absence of papilledema.

Lumbar puncture is contraindicated in patients who take anticoagulant medication or have a bleeding disorder. Lumbar puncture can cause intraspinal bleeding, which can compress the cauda equina. If CSF analysis is necessary, the patient can be pretreated with fresh frozen plasma, platelets, cryoprecipitate, or the specific factor to correct the hematologic abnormality.

Lumbar puncture should not be performed if there is infection at the puncture site. This contraindication avoids introducing the infection into the subarachnoid space. In case of infection, a lateral C1-C2 puncture can be performed by a neurosurgeon to obtain the CSF sample. Despite these contraindications, lumbar puncture is a safe and easy procedure.

Explain the procedure to the patient and provide emotional support throughout the procedure to reduce the patient’s apprehension. The key to a successful lumbar puncture is proper positioning of the patient. The patient should be in the lateral decubitus position, with the back at the edge of the table or bed to provide back support. The patient’s shoulders should be aligned and the spine parallel to the edge of the bed. The patient should assume the fetal position, bringing the knees to the chin. The L3-L4 vertebral interspace is in the middle at the level of the superior iliac crest (Figure 2.1). In adults, the caudal end of the spinal cord is at vertebral level L1-L2, so vertebral level L3-L4 or the 1 above or below can be punctured safely. In infants and children, the caudal end of the spinal cord is lower relative to the vertebral column, and it is best to use the L4-L5 or L5-S1 vertebral interspace.


Figure 2.1. Lumbar Puncture. A, Position of patient and location of L3-L4 interspace (red dashed line). B, Longitudinal section through the vertebral column showing the path of the lumbar needle. C, Lumbar needle in the L3-L4 interspace.

Figure 2.1. Lumbar Puncture. A, Position of patient and location of L3-L4 interspace (red dashed line). B, Longitudinal section through the vertebral column showing the path of the lumbar needle. C, Lumbar needle in the L3-L4 interspace.

(Adapted from Patten J. Neurological differential diagnosis. New York [NY]: Springer-Verlag; ©1977. p. 262, 264. Used with permission.)

Perform the puncture with strict aseptic technique. Cleanse the skin with an iodine solution 3 times, starting at the puncture site and washing outward in concentric circles. Often, alcohol is used to remove the iodine to avoid introducing iodine into the subarachnoid space. Apply the sterile drape, and prepare all the equipment before inserting the needle. To anesthetize the skin, use a small intradermal needle to inject lidocaine into a small wheal over the puncture site. Warn the patient that this step can cause a stinging sensation. Deeper structures can be anesthetized, but this may be more uncomfortable for the patient than the spinal needle.

For adults, use a 20-gauge lumbar puncture needle with stylet because 1) it is rigid enough to penetrate the ligamentum flavum, 2) it provides for an accurate pressure reading, and 3) it is large enough to collect CSF rapidly. The stylet needs to be in place on insertion to avoid the rare complication of implanting an epidermoid tumor in the subarachnoid space. The needle with stylet should be directed with the bevel parallel to the long axis of the spine to spread or to split the dural fibers that run longitudinally. This minimizes leakage of the CSF into the subdural space. Steadily direct the needle toward the umbilicus until there is a “give,” or a reduction in resistance, as the needle pierces the dura mater.

Remove the stylet, and check for CSF return. If no fluid is obtained, rotate the needle. If no fluid appears, replace the stylet and advance the needle in small, 1- to 2-mm increments, checking for CSF with each advance. Inserting the needle too far injures the venous plexus anterior to the spinal canal; this is the most common cause of a traumatic tap. If bone is encountered, the needle should be withdrawn to the level of the skin (to avoid the same path of the first puncture) and redirected. Repeated puncture of the skin should be avoided because of the increased risk of infection and subcutaneous bleeding. If the patient complains of pain down the leg, the needle needs to be directed more medially. If the patient cannot tolerate lying on the side or cannot be positioned properly, the procedure can be done with the patient sitting, leaning forward over a table. This position does not permit an accurate pressure reading, but the patient can be repositioned in the lateral decubitus position for this measurement. If the puncture is not successful, a different interspace can be used or the procedure can be performed under fluoroscopic guidance.

After CSF has been obtained, attach the manometer to the hub of the needle and record the opening pressure. The patient should be encouraged to relax and to breathe normally to avoid a falsely high pressure reading. The meniscus should show minimal fluctuation related to pulse and respiration. Collect the CSF in 4 separate vials (labeled 1 through 4), and remove the needle without the stylet to avoid trapping any nerve roots. Traditionally, the patient was instructed to remain flat or prone for some time to reduce the risk of post–lumbar puncture headache. However, studies have shown that remaining flat is not an important factor. In a large outpatient study, thin young women had the highest risk for post–lumbar puncture headache. The duration of the recumbence and the amount of CSF obtained did not influence the risk of headache.

Post–lumbar puncture headache is the most frequent complication of lumbar puncture, with a reported frequency of 10% to 38%. The use of an atraumatic spinal needle and a small needle size reduces the risk of post–lumbar puncture headache. The headache usually responds to a short period of bed rest. A persistent headache for more than 2 days can be treated with an epidural injection of autologous blood at the site of the puncture. Other complications of lumbar puncture are rare and include diplopia, infection, backache, and radicular symptoms.

A traumatic tap, that is, bleeding into the subarachnoid space from injury to small blood vessels, can compromise the interpretation of CSF results. A CSF sample with traumatic blood clears as the fluid is collected, and fewer erythrocytes are found in vial 4 than in vial 1. The opening pressure in a traumatic tap is normal, compared with the pressure in cases of subarachnoid hemorrhage or meningitis. The supernatant of centrifuged CSF should be clear if the tap was traumatic and xanthochromic (yellow) if blood has been present for several hours and has undergone hemolysis. Blood from a traumatic tap will increase the number of erythrocytes and leukocytes and the amount of protein in the CSF. The formula used to estimate the increase is the following: 700 erythrocytes can account for an increase of 1 leukocyte and 1 mg of protein.

Analysis of CSF is essential for diagnosing many disorders of the CNS (Table 2.1). Also, the removal of CSF can be therapeutic, as in pseudotumor cerebri and normal-pressure hydrocephalus. In a patient with normal-pressure hydrocephalus, an improvement in gait after removal of CSF indicates that a shunt may be beneficial. The clinical value of CSF analysis is discussed further in relation to neurologic infections and neuro-oncology (Chapters 13 and 14).

Table 2.1. Features of the Cerebrospinal Fluid in Various Diseases

Condition

Clinical Findings

Appearance

Opening Pressure

Protein

Glucose

Cell Count

Normal

Clear, colorless

50–200 mm H2O

15–45 mg/100 mL

45–80 mg/mL (2/3 that of serum)

  • RBCs, 0

  • WBCs, 0–5 μ‎L (lymphocytes or monocytes)

Subarachnoid hemorrhage

“Worst headache of life,” stiff neck, negative CT

Blood tinged, xanthochromic

Increased

Increased

Normal

Same as blood

Bacterial meningitis

Headache, mental status change

Opalescent, purulent

Increased

Increased

Decreased

Increased number of WBCs (PMNs)

Viral meningitis

Headache, mental status change

Normal or opalescent

Increased or normal

Increased

Decreased

Increased number of WBCs (lymphocytes)

Carcinomatous meningitis

Headache, cranial nerve signs, seizures

Cloudy

Increased or normal

Increased

Decreased

Increased number of WBCs, malignant cells

Multiple sclerosis

Multiple signs and symptoms

Normal

Normal

Normal, increased IgG

Normal

Normal or increased number of lymphocytes

Pseudotumor cerebri

Headache, papilledema, normal CT

Normal

Increased

Normal

Normal

Normal

Guillain-Barré syndrome

Ascending paralysis

Normal

Normal

Increased

Normal

Normal

Abbreviations: CT, computed tomography; IgG, immunoglobulin G; PMNs, polymorphonuclear neutrophils; RBCs, erythrocytes; WBCs, leukocytes.

Adapted from Adams AC. Neurology in primary care. Philadelphia (PA): FA Davis; ©2000. p. 31. Used with permission of Mayo Foundation for Medical Education and Research.

Electroencephalography

An important feature of EEG is that it is a physiologic test that provides information about function instead of structure. An example that emphasizes this point is the case of a child with a head injury and altered behavior and normal findings on neuroimaging. Normal neuroimaging results cannot explain the child’s abnormal behavior. However, EEG identifies the problem, namely, nonconvulsive status epilepticus amenable to anticonvulsant therapy. EEG is noninvasive and relatively inexpensive. It is an extension of the clinical examination, and the information obtained with EEG should be interpreted in the context of the patient’s clinical presentation. Normal EEG findings do not exclude neurologic disease, and abnormal EEG findings may be of no clinical consequence.

The quality of the test results depends on the skill of the EEG technician and the electroencephalographer. Accreditation of the EEG laboratory and certification of the technician and electroencephalographer indicate that the recording meets acceptable standards. Eighteen to 21 recording channels are recommended. An electrocardiogram line should be used because it provides useful information about cardiac rhythm. This feature is particularly helpful when evaluating a patient who has spells or other transient disorders. Activation procedures, including hyperventilation, intermittent photic stimulation, and sleep, should be part of the EEG study to increase the frequency of epileptogenic activity. Hyperventilation is an activation procedure that is particularly useful in patients with absence seizures. Hyperventilation should be used with care in patients who have cardiopulmonary disease.

EEG is indispensable in the evaluation of patients who have seizures. It can be critical in diagnosing seizures, determining the probability of recurrent seizures, and selecting the best treatment for seizures. The sensitivity of a single EEG recording for identifying specific epileptiform activity is reportedly about 50%. This increases to about 90% with 3 EEG recordings. Prolonged EEG recording with video monitoring increases diagnostic sensitivity. Ambulatory EEG monitoring can be useful, but excessive artifact can complicate these studies.

EEG can be clinically useful for many transient disorders or spells. In disorders of altered consciousness, EEG can determine whether the process is diffuse, focal, or multifocal. Serial EEG recordings can help determine prognosis in coma and encephalopathy. EEG may be useful in distinguishing between dementia and pseudodementia, diagnosing sleep disorders, and determining brain death. When requesting an EEG, the clinical question should be stated clearly and the electroencephalographer should attempt to answer the question within the limitations of the test.

The normal awake EEG is characterized by an alpha (8–13 Hz) rhythm recorded over the posterior head region; this rhythm attenuates with eye opening (Figure 2.2B). EEG sleep activity is illustrated in Figure 2.2C and Figure 2.2D. Abnormalities seen on EEG include slowing, asymmetry, suppression or loss of EEG activity, and epileptiform activity (spikes, sharp waves, and spike-and-wave). Common EEG findings and their anatomical and clinical correlates are summarized in Table 2.2. EEG abnormalities and abnormal patterns are shown in Figures 2.3 and 2.4.


Figure 2.2. A, Placement of Electroencephalographic (EEG) Electrodes. A indicates earlobe; C, central; F, frontal; O, occipital; P, parietal. Lower case letters: p, polar; z, midsagittal. Even numbers, right hemisphere; odd numbers, left hemisphere. B, Normal awake EEG pattern. Note alpha rhythm recorded over the posterior head region (P3-O1, and P4-O2) in an awake patient with eyes closed. The rhythm attenuates when the eyes are opened. C, Normal sleep EEG pattern with V waves (these waves are maximal over the vertex region and resemble the letter “V”) and spindles (10–14-Hz sinusoidal activity). D, Comparison of EEG patterns of wakefulness and different levels of sleep. The awake EEG is recorded from the occipital areas, with eyes closed. The rapid eye movement (REM) sleep pattern resembles the awake EEG pattern with eyes open.

Figure 2.2. A, Placement of Electroencephalographic (EEG) Electrodes. A indicates earlobe; C, central; F, frontal; O, occipital; P, parietal. Lower case letters: p, polar; z, midsagittal. Even numbers, right hemisphere; odd numbers, left hemisphere. B, Normal awake EEG pattern. Note alpha rhythm recorded over the posterior head region (P3-O1, and P4-O2) in an awake patient with eyes closed. The rhythm attenuates when the eyes are opened. C, Normal sleep EEG pattern with V waves (these waves are maximal over the vertex region and resemble the letter “V”) and spindles (10–14-Hz sinusoidal activity). D, Comparison of EEG patterns of wakefulness and different levels of sleep. The awake EEG is recorded from the occipital areas, with eyes closed. The rapid eye movement (REM) sleep pattern resembles the awake EEG pattern with eyes open.

(A and B adapted from Westmoreland BF. Clinical EEG manual. [cited 2015 Feb 18]. Available from: http://mayoweb.mayo.edu/man-neuroeeg/index.html. Used with permission of Mayo Foundation for Medical Education and Research. D from Benarroch EE, Westmoreland BF, Daube JR, Reagan TJ, Sandok BA. Medical neurosciences: an approach to anatomy, pathology, and physiology by systems and levels. 4th ed. Philadelphia [PA]): Lippincott Williams & Wilkins; ©1999. p. 304. Used with permission of Mayo Foundation for Medical Education and Research.)

Table 2.2. Localization and Clinical Correlates of Common EEG Findings

EEG Finding

Localization

Clinical Correlate

Generalized spike-and-wave activity

Diffuse cortex

  • Absence seizure

  • Generalized tonic-clonic seizure

Focal spike-and-wave activity, sharp waves

Focal cortex

Partial epilepsy

Diffuse slowing

Diffuse cortex

Encephalopathy

Focal slowing

Focal cortex

Focal structural lesion

Periodic lateralized epileptiform discharges (PLEDs)

Localized or hemispheric dysfunction

Acute or subacute process (eg, herpes encephalitis)

Triphasic waves

Diffuse cortex

Encephalopathy (eg, hepatic)

Generalized periodic and slow wave complex

Diffuse cortex

Creutzfeldt-Jakob disease

Burst suppression

Diffuse cortex

Post cardiopulmonary arrest

Abbreviation: EEG, electroencephalographic.

Adapted from Adams AC. Neurology in primary care. Philadelphia (PA): FA Davis; ©2000. p 32. Used with permission of Mayo Foundation for Medical Education and Research.


Figure 2.3. Electroencephalogram (EEG) Abnormalities. A, Epileptiform discharges. B, Generalized pattern. The generalized 3 per second spike and wave is the EEG pattern typical of absence seizures. C, Focal pattern. Right temporal spike is an EEG pattern seen in complex focal seizures originating on the right. T indicates temporal. Other electrodes are as defined in the legend to Figure 2.2.

Figure 2.3. Electroencephalogram (EEG) Abnormalities. A, Epileptiform discharges. B, Generalized pattern. The generalized 3 per second spike and wave is the EEG pattern typical of absence seizures. C, Focal pattern. Right temporal spike is an EEG pattern seen in complex focal seizures originating on the right. T indicates temporal. Other electrodes are as defined in the legend to Figure 2.2.

(Adapted from Westmoreland BF. Clinical EEG manual. [cited 2015 Feb 18]. Available from: http://mayoweb.mayo.edu/man-neuroeeg/index.html. Used with permission of Mayo Foundation for Medical Education and Research.)


Figure 2.4. Abnormal Electroencephalographic (EEG) Patterns. A, Burst suppression pattern consists of periodic bursts of abnormal activity separated by periods of electrocerebral silence. This pattern indicates severe brain injury, eg, after cardiopulmonary arrest. B, PLEDs (periodic lateralized epileptiform discharges) represent an acute epileptic focus in a focal or lateralized pattern. This pattern often develops after herpes simplex encephalitis or vascular lesions. C, Periodic sharp waves are typical of Creutzfeldt-Jakob disease. D, Triphasic waves is an EEG pattern associated with hepatic encephalopathy. Electrodes are as defined in the legend to Figure 2.2.

Figure 2.4. Abnormal Electroencephalographic (EEG) Patterns. A, Burst suppression pattern consists of periodic bursts of abnormal activity separated by periods of electrocerebral silence. This pattern indicates severe brain injury, eg, after cardiopulmonary arrest. B, PLEDs (periodic lateralized epileptiform discharges) represent an acute epileptic focus in a focal or lateralized pattern. This pattern often develops after herpes simplex encephalitis or vascular lesions. C, Periodic sharp waves are typical of Creutzfeldt-Jakob disease. D, Triphasic waves is an EEG pattern associated with hepatic encephalopathy. Electrodes are as defined in the legend to Figure 2.2.

(A, C, and D adapted from Westmoreland BF. Clinical EEG manual. [cited 2015 Feb 18]. Available from: http://mayoweb.mayo.edu/man-neuroeeg/index.html. Used with permission of Mayo Foundation for Medical Education and Research. B from Westmoreland BF. Epileptiform electroencephalographic patterns. Mayo Clin Proc. 1996;71:505-11. Used with permission of Mayo Foundation for Medical Education and Research.)

Evoked Potentials

An evoked potential is an electrical response of the nervous system to an external stimulus. Evoked potentials measure conduction in nerve pathways from the periphery through the CNS. In clinical practice, this includes the visual, auditory (or brainstem), and somatosensory pathways. Evoked potentials are noninvasive tests that provide valuable physiologic information about the nervous system. For example, they are sensitive to demyelination and have been used to detect clinically silent lesions in patients with multiple sclerosis.

Visual evoked potentials extend the physical examination of the visual system and are useful in diagnosing optic nerve disease and determining the likelihood of the recovery of vision. If an ophthalmologic problem has been excluded, abnormal visual evoked potentials reportedly are 100% sensitive in detecting optic neuritis even after the recovery of vision and can be useful in assessing visual function in infants and uncooperative patients. The visual evoked potential in response to a pattern reversal stimulus in a patient with left eye optic neuritis is shown in Figure 2.5.


Figure 2.5. Visual Evoked Potential With Pattern Reversal Stimulus. The visual evoked response is prolonged on the left (left eye optic neuritis), compared with the right (right eye normal).

Figure 2.5. Visual Evoked Potential With Pattern Reversal Stimulus. The visual evoked response is prolonged on the left (left eye optic neuritis), compared with the right (right eye normal).

(Adapted from Mancall EL, editor. Evoked potentials. Continuum Lifelong Learn Neurol. 1998 Oct;4 [5]‌:58. Used with permission.)

Auditory, or brainstem, evoked potentials are sensitive to anatomical disturbances of brainstem pathways. These potentials are not affected by the level of consciousness, drugs, or metabolic disturbances. Auditory evoked potentials can be used to assess brainstem pathways in infants and in unresponsive or uncooperative patients. They also are helpful in evaluating complaints of vertigo, hearing loss, and tinnitus. Auditory evoked potentials can identify hearing impairment in infants and are used to screen for acoustic neuromas. They also are valuable in intraoperative monitoring during posterior fossa surgery. An abnormal brainstem auditory response on the left side in a patient who had an acoustic neuroma is shown in Figure 2.6.


Figure 2.6. Brainstem Auditory Evoked Potential. Note the delay of peaks III and V on the left compared with those on the right. This abnormality on the left indicates a brainstem lesion.

Figure 2.6. Brainstem Auditory Evoked Potential. Note the delay of peaks III and V on the left compared with those on the right. This abnormality on the left indicates a brainstem lesion.

(Adapted from Mancall EL, editor. Evoked potentials. Continuum Lifelong Learn Neurol. 1998 Oct;4 [5]‌:57. Used with permission.)

Somatosensory evoked potentials are useful in assessing peripheral nerves, the spinal cord, and cerebral cortex. They can be used to confirm the presence of an organic disease process in a patient who has sensory complaints. They also are valuable in intraoperative monitoring to protect neural structures.

Nerve Conduction Studies and EMG

It cannot be overemphasized that electrophysiologic studies are extensions of the clinical examination and that the quality of the studies is operator dependent. EMG can be indispensable in the evaluation and treatment of patients who have muscle, neuromuscular junction, peripheral nerve, or motor neuron disease. It provides functional information and often supplements structural information from such tests as CT and MRI. EMG may provide the most critical information in the case of a patient with low back pain and radicular symptoms in whom MRI shows multiple-level degenerative changes. Many abnormalities seen on MRI are not clinically significant. The results of an EMG will indicate which level is symptomatic. Also, EMG is essential for confirming the diagnosis of motor neuron disease.

When ordering EMG, it is important to understand the kind of information that can be obtained and the limitations of the test. EMG results will be more meaningful if the clinical question is clear and the electromyographer knows the clinical question to be answered. The timing of the study is critical. Abnormalities of peripheral nerves may not be demonstrated with EMG until 2 to 6 weeks after an acute injury. It is helpful if the patient is prepared for the test and understands what it involves.

Nerve Conduction Studies

Nerve conduction can be measured in sensory and motor nerves. Nerve conduction studies can test only medium- to large-diameter myelinated fibers. These include motor fibers and the sensory fibers that convey vibratory sensation and proprioception. Small unmyelinated fibers that conduct pain and temperature sensations cannot be evaluated with EMG. Patients with small-fiber neuropathies often have normal EMG findings.

The motor nerves that are commonly tested are the median, ulnar, peroneal, and posterior tibial nerves. A recording electrode is placed on the muscle, and the nerve is stimulated with a mild electric shock at distal and proximal sites (Figure 2.7). Important values include the distal latency, conduction velocity, and conduction amplitude. The time measured from stimulating the nerve at the distal site to contraction of the muscle is the distal latency. The time measured from stimulating the nerve at the proximal site to contraction of the muscle is the proximal latency. For the median nerve, a prolonged distal latency supports the diagnosis of carpal tunnel syndrome. Conduction time is the speed of the nerve impulse. It is calculated by dividing the length of the nerve segment by the difference between the distal and proximal latencies.


Figure 2.7. Setup for Recording Median Nerve Conduction Velocity. Motor nerve conduction velocity, reported in meters per second, =  



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Figure 2.7. Setup for Recording Median Nerve Conduction Velocity. Motor nerve conduction velocity, reported in meters per second, = D i s t a n c e P r o x i m a l l a t e n c y D i s t a l l a t e n c y .

(Adapted from Adams AC. Neurology in primary care. Philadelphia [PA]: FA Davis; ©2000. p. 33. Used with permission of Mayo Foundation for Medical Education and Research.)

Conduction velocity is related to the diameter (myelination) of the nerve. A slow nerve conduction velocity indicates a demyelinating peripheral neuropathy. The amplitude of the motor unit potential is related to the number of axons. A decrease in amplitude indicates an axonal polyneuropathy (Table 2.3).

Table 2.3. Components of Nerve Conduction Studies

Component (Unit of Measure)

Is a Function of

Is Abnormal in

Distal latency (milliseconds)

Conduction rate

Compression neuropathies (carpal tunnel syndrome)

Amplitude

  • Motor (millivolts)

  • Sensory (microvolts)

Number of axons

Axonal neuropathies (diabetic neuropathy)

Conduction velocity (meters/second)

Axon diameter, myelination

Demyelinating neuropathies (hereditary sensory motor neuropathy, chronic inflammatory demyelinating polyradiculoneuropathy)

Adapted from Adams AC. Neurology in primary care. Philadelphia (PA): FA Davis; ©2000. p 34. Used with permission of Mayo Foundation for Medical Education and Research.

Muscle Studies

The electrical activity of muscles is recorded by inserting a small needle electrode into the muscle. Information is obtained during the insertion of the needle, with the muscle at rest, and with voluntary contraction. The clinical indication for EMG determines which muscles are tested. To facilitate the study, provide the electromyographer with the necessary clinical information. The electromyographer needs to know if the patient is taking an anticoagulant or has a bleeding diathesis.

The brief discharge that occurs when the needle is inserted into the muscle is called insertional activity. Insertional activity is increased in neurogenic disorders, such as peripheral neuropathies, that cause abnormal excitability of muscle. At rest, a normal muscle has no spontaneous activity (excluding end plate activity). Abnormal spontaneous activity is seen in neurogenic lesions associated with denervation and inflammatory myopathies. Motor unit action potentials are recorded when the muscle is contracted voluntarily. These potentials are analyzed for amplitude, duration, phases, and recruitment. With continued muscle contraction, the motor units summate and the response is referred to as the interference pattern. EMG features of clinical disorders are summarized in Figure 2.8.


Figure 2.8. Comparison of Normal Electromyographic Patterns With Those of Neurogenic Disorders, Myopathy, and Polymyositis.

Figure 2.8. Comparison of Normal Electromyographic Patterns With Those of Neurogenic Disorders, Myopathy, and Polymyositis.

(Adapted from Kimura J. Electrodiagnosis in diseases of nerve and muscle: principles and practice. 4th ed. New York [NY]: Oxford University Press; ©2013. p. 364. Used with permission.)

Magnetic Resonance Imaging

MRI is the imaging test preferred for evaluating the posterior fossa, neoplastic disease, meningeal disease, subacute hemorrhage, seizures, and demyelinating disease. Images can be obtained in several planes, including the coronal, axial, and sagittal planes (Figure 2.9). Adverse reactions to the contrast agent gadolinium are rare. MRI is more expensive than CT and is insensitive to calcification. The clinical situations for which MRI or CT is the preferred imaging study are summarized in Table 2.4. An absolute contraindication to MRI is the presence of magnetic intracranial aneurysm clips, cardiac pacemakers, and implantable cardioverter-defibrillators. However, some new protocols and new devices may allow for these studies in selected patients. Consultation with radiology is recommended. Women in the first trimester of pregnancy and metal workers with metal fragments in the eye are usually excluded from the test.


Figure 2.9. Magnetic Resonance Imaging of the Brain in the Sagittal (A), Coronal (B), and Axial (C) Planes.

Figure 2.9. Magnetic Resonance Imaging of the Brain in the Sagittal (A), Coronal (B), and Axial (C) Planes.

Table 2.4. Indication for Selecting CT or MRI

Indication

Preferred Test

Acute trauma

CT

Acute stroke (intracranial hemorrhage)

CT

Cost

CT

Bone, calcification

CT

Demyelinating disease

MRI

Mental status changes after trauma

MRI

Seizures

MRI

Tumor

MRI

Metastatic disease

MRI

Meningeal disease

MRI

Dementia

MRI

Uncooperative or medically unstable patient

CT

Abbreviations: CT, computed tomography; MRI, magnetic resonance imaging.

Adapted from Adams AC. Neurology in primary care. Philadelphia (PA): FA Davis; ©2000. p 37. Used with permission of Mayo Foundation for Medical Education and Research.

The principles of magnetic resonance are complex, but the images result from the varying intensities of radio wave signals emanating from the tissue in which hydrogen nuclei have been excited by a radiofrequency pulse. The signal intensity (white or dark) on the MRI is determined by the way protons revert to the resting state after a radiofrequency pulse (relaxation time, T1 and T2), the concentration of protons in the tissue (proton density), and flow. Contrast on magnetic resonance can be manipulated by changing pulse sequence parameters. The 2 that are most important are echo time and repetition time. A discussion of the technique is beyond the scope of this text, but it is important to know from a clinical perspective that different techniques can be used to enhance imaging of the nervous system.

Usually, both T1-weighted images and T2-weighted images are used in imaging the brain and spine. T1-weighted images are useful for analyzing anatomical detail. T2-weighted images are very sensitive to the presence of increased water. Most brain lesions have long T2 and long T1 so they will be of high signal, or white, on T2-weighted images and low signal, or dark, on T1-weighted images (Table 2.5).

Table 2.5. Pathologic Appearance on Different Magnetic Resonance Imaging Sequences

Feature

T1-Weighted Image

T2-Weighted Image

PD/FLAIR Imaging

Acute ischemia

Gray

Dark

Dark

Cyst

Dark

White

Dark

Fat

White

Dark

White

Solid mass

Dark

White

White

Subacute blood

White

White

White

Abbreviations: FLAIR, fluid-attenuated inversion recovery; PD, proton density.

Other sequences used in imaging the CNS include proton density, fluid-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (Figure 2.10). FLAIR sequences minimize signals from CSF and increase the sensitivity for detecting small tumors, vascular malformations, and mesial temporal sclerosis. Diffusion-weighted imaging detects random movements of water protons and is sensitive to early cerebral ischemia (Figure 2.10). Current steady-state free precession sequences like fast imaging employing steady-state acquisition are excellent for evaluation of cranial nerves.


Figure 2.10. Normal Brain Appearance Magnetic Resonance Imaging. A–F, Different sequences. CSF indicates cerebrospinal fluid; T1WI, T1-weighted image; T2WI, T2-weighted image.

Figure 2.10. Normal Brain Appearance Magnetic Resonance Imaging. A–F, Different sequences. CSF indicates cerebrospinal fluid; T1WI, T1-weighted image; T2WI, T2-weighted image.

MRI is also advantageous for imaging flowing blood. Magnetic resonance angiography, a noninvasive method for evaluating cerebral vasculature, can detect aneurysms as small as 3 to 4 mm (Figure 2.11). MRI is a rapidly evolving specialty, and many clinical advances can be anticipated.


Figure 2.11. Magnetic Resonance Angiography of the Cerebral Circulation. A, Anterior-posterior view. B, Inferior view. ACA indicates anterior cerebral artery; ACOM, anterior communicating artery; IC, internal carotid artery; MCA, middle cerebral artery; PCA, posterior cerebral artery; PCOM, posterior communicating artery.

Figure 2.11. Magnetic Resonance Angiography of the Cerebral Circulation. A, Anterior-posterior view. B, Inferior view. ACA indicates anterior cerebral artery; ACOM, anterior communicating artery; IC, internal carotid artery; MCA, middle cerebral artery; PCA, posterior cerebral artery; PCOM, posterior communicating artery.

Angiography

Magnetic resonance angiography is becoming the preferred method for evaluating cerebrovascular disease. However, conventional angiography is still a valuable diagnostic test in the assessment of aneurysms, vascular malformations, and vasculitis. Advances have included safer digital imaging, smaller catheters, and improved radiographic contrast agents. The risk of serious morbidity has decreased, and the rate of stroke resulting from the procedure should be less than 0.5% when it is performed by a skilled practitioner. Therapeutic uses have expanded to include use in thrombolytic therapy. The most common adverse effect of angiography is groin hematoma.

Myelography

Myelography is a radiographic test that allows the spine to be visualized after a radiopaque substance has been injected into the spinal subarachnoid space. The test is helpful in diagnosing disease of the spine, such as herniated disk and spinal stenosis. Myelography is invasive and has the same contraindications as lumbar puncture. MRI of the spine has the major advantage of being noninvasive; also, it may be more sensitive for detecting metastatic disease of the spine and spinal cord compression syndromes. With improvement in contrast agents, myelography has become safer, with fewer adverse reactions. Myelography may provide additional information when the results of MRI or CT are ambiguous.

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