More tests from the above link,
Electromyogram (EMG)
A needle electrode is inserted in the muscle. Normally there is no muscle activity at rest, but with minimal voluntary contraction, individual motor unit potentials are seen. These represent the summation of the membrane action potentials of many muscle fibers, all innervated by the same anterior horn cell (the motor unit). With increasing contraction, more motor units are recruited, the firing rate increases, and a dense interference pattern is seen in which the baseline of the EMG is no longer visible.
Changes with neuropathy
When the muscle is partially denervated, there are changes in the excitability of muscle fibers, so that after about three weeks muscle fibers may fire at rest (fibrillations). If denervated fibers are reinnervated by neighboring healthy nerve axons (a process that takes place over months), motor units are formed that are larger than normal. As the number of motor units decreases, the interference pattern seen with maximal contraction becomes less dense, and large polyphasic cross innervation units are seen.
Changes with myopathy
The number of motor units remains normal, and therefore the interference pattern is normal except in the very late stages. The individual units are smaller because some muscle fibers have dropped out. The motor unit potentials are, therefore, on the average, smaller in amplitude and shorter in duration. More units must be fired to produce a particular strength of contraction, so the full interference pattern is achieved earlier. Polyphasic potentials are also seen. The EMG picture of brief, small-amplitude, abundant, polyphasic potentials (BSAPP) is characteristic (although not pathognomonic) of myopathy. Although usually the muscle is silent at rest, fibrillations can occur, and are often seen in persons with polymyositis, perhaps a result of denervation caused by damage to the intramuscular nerves.
In normal persons muscle activity ceases abruptly with muscle relaxation. In patients with myotonia, repetitive afterdischarges are seen. This correlates with clinical myotonia (see Chapter 21 ) but is more sensitive. Cases of myotonic dystrophy can therefore be diagnosed by EMG before clinically obvious myotonia is present.
Neuromuscular junction
Repetitive stimulation of a nerve produces little attenuation of the summated muscle action potential at rates of 3 to 30 per second. In persons with myasthenia gravis, however, this attenuation is marked because neuromuscular transmission is marginal at the start. Conversely, in the "myasthenic" syndrome associated with carcinoma (the Eaton-Lambert syndrome), repetitive stimulation augments the muscle response.
Chapter 11 - Neurologic Tests
Many tests are used specifically for the evaluation of neurologic illnesses (Table 11-1). The general physician should be familiar with the diagnostic capabilities of all these tests and should be able to interpret the results of the lumbar puncture.
Lumbar Puncture
Technique
The technique of lumbar puncture is learned in the ward, so only a few points are made here. Spinal taps should not be done above the L2-3 interspace because the spinal cord may be present above this level. If the flow of spinal fluid is not brisk, the following check is simple (Figure 11-1): The manometer is tilted horizontally to increase the flow and then brought back to the vertical position so that the fluid falls to the true spinal fluid pressure. If this maneuver fails to increase the flow, the needle is not properly placed or a nerve root has blocked the needle. Fluid should not be aspirated because this may trap and damage nerve roots. If the initial CSF pressure is high (more than 180 mm H2O), the physician should try to let it fall without removing fluid; the patient should be encouraged to relax, and their neck and legs should, if necessary, be unflexed (thus reducing venous pressure). S/he should not be asked to hyperventilate (this causes cerebral vasoconstriction and lowers even truly high CSF pressures). S/he should be reassured, made comfortable, and allowed to rest for one minute (not much more). Even if the pressure is high, enough CSF should be removed for the performance of routine tests (about 6-9 cc; 2-3 cc in each tube).
Examination of the fluid
Cell counts should be made in the first and last tubes. The fluid is then examined for color (compare with a tube of water against a white background) and then analyzed for protein and sugar. The whole CSF or the sediment can be stained for microorganisms (in appropriate cases). Analysis for bacterial or fungal antigens or polymerase chain reaction for viruses or tuberculous bacilli should be employed depending on the clinical situation. A separate tube (usually tube 2) should be sent for cultures. Fungal and AFB cultures should be requested when indicated. CSF protein electrophoresis and measurement of IgG synthesis (which requires comparison of spinal fluid with a blood sample) can give hints to the presence of an immune/inflammatory condition. Myelin basic protein concentration can confirm damage to CNS myelin.
Interpretation
CSF pressure
Although elevated CSF pressure should raise the question of an intracranial mass lesion, intracranial pressure may also increase when there is an obstruction to the flow of CSF or when the intracranial venous pressure rises (Table 11-2). Reduced CSF pressure can be artifactual (needle not properly placed, or blocked by a nerve root - check flow) or caused by CSF block (as by a spinal tumor or cerebellar herniation through the foramen magnum), general dehydration, prior lumbar punctures (the result of CSF leakage through puncture holes in the arachnoid and dura), or a posttraumatic or spontaneous CSF leak.