Abstract
The neurologist has a continuously expanding arsenal of ancillary investigations at hand. Good clinical skills are mandatory to put the patient on the right diagnostic track and to ensure correct interpretations of the results. Every investigation ordered should serve a specific purpose and help to answer a well-considered and well-formulated question. Close cooperation and, preferentially, personal communication with appropriate colleagues such as radiologists, neurophysiologists, and geneticists are mandatory. Given the book’s focus on bedside skills, the following overview of neuroimaging, neurophysiology, ultrasound techniques, laboratory evaluations of blood and cerebrospinal fluid, genetic testing, and neuropsychological evaluation is short but covers many elementary technical and clinical facts relevant to the general neurologist. Clinical neurophysiology is discussed in somewhat greater detail, since it is the domain of the neurologist in many countries.
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Notes
- 1.
Following a lumbar puncture, diffuse meningeal contrast enhancement in the lower spine may be seen for days or weeks, and, although not pathological, this may lead to diagnostic confusion.
- 2.
For instance, a C8 nerve root lesion may lead to EMG abnormalities in the latissimus dorsi (thoracodorsal nerve), triceps, extensor digitorum communis, extensor indicis proprius (radial nerve), abductor pollicis brevis (median nerve), flexor carpi ulnaris, and flexor digitorum profundus muscles of the fourth and fifth digits (ulnar nerve), as well as in the small hand muscles (ulnar and median nerve). In contrast, an ulnar nerve lesion will leave the latissimus dorsi, triceps, extensor digitorum communis, extensor indicis proprius, and abductor pollicis brevis muscles intact.
- 3.
Needle examination of the sternocleidomastoid muscles carries a sensitivity similar to examination of the tongue in patients with bulbar symptoms and may be better tolerated by the patient.
- 4.
In contrast to Doppler sonography, CT/MR angiography is more time-consuming but allows complete imaging of the intracranial and neck vessels, including the aortic arch, which is why CT/MR angiography can also detect stenoses distally and proximally from the carotid artery bifurcation.
- 5.
Tau proteins are abundant in the CNS and essential for stabilizations of microtubules in neurons. High total tau levels can be used as a marker of cortical axonal degeneration. Phosphorylation of tau is believed to be specific for AD and related tauopathies. Beta-amyloid is the main constituent of amyloid plaques in the brains of patients with AD. Since amyloid accumulates within the neurons and cerebral vessel, its amount in CSF is decreased in AD.
- 6.
Similar to tau protein, NFL light protein is an important component of neuronal axons. The CSF level of NFL light protein increases in disorders with neuronal damage and axonal degeneration and correlates with the amount of damage.
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Kondziella, D., Waldemar, G. (2023). Ancillary Investigations. In: Neurology at the Bedside. Springer, Cham. https://doi.org/10.1007/978-3-031-43335-1_5
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