Neuroanatomy is primarily an anatomical rather than a clinical textbook. Neuroanatomy is, however, the foundation of clinical neurological diagnosis. This is because the clinical syndromes arising from lesions within the neuromuscular system are determined by the topographical location of the lesion, rather than by its cause. Thus, by combining knowledge of neuroanatomy with the practical skills of the clinical examination, the site of the lesion can be determined with great accuracy at the bedside and before the application of sophisticated investigations. Once the clinical syndrome is defined and the site of the lesion within the nervous system located, it is possible to infer the cause of the lesion by a careful consideration of the evolution of the patient’s symptoms, obtained by clinical history-taking. The ultimate diagnosis is reached by applying appropriate investigations in order to clarify the site and cause of the lesion.
In order to exemplify this diagnostic process, a series of problem-solving tasks is presented. These provide sufficient information concerning the clinical neurological findings on examination to permit deduction of the site of the lesion within the neuromuscular system.
Throughout the text, simplified summaries of the major anatomical–clinical syndromes are presented diagrammatically, following the conventional neurological examination of cranial nerves, motor function, reflexes, sensation, coordination and mental state, described in textbooks of clinical methods. These figures follow a standard style exemplified by Figure 17.1.
Figure 17.1 Prototypical figure for illustration of major syndromes of the neuromuscular system.
The figures from the foregoing text that summarise the major anatomical–clinical syndromes are reproduced below (Figs 17.2-17.13), with the omission of the small inset diagram that identifies the site of the lesion. In each case, the task is to study the findings of the clinical examination and thereby deduce the location of the lesion. The aetiology of the lesions can also be inferred from study of Figures 1.31–1.39Figure 1.31Figure 1.32Figure 1.33Figure 1.34Figure 1.35Figure 1.36Figure 1.37Figure 1.38Figure 1.39 (Aetiology of neurological disease; Ch. 1) which link aetiologies to neuroanatomical sites.
Solutions to task
Figure 17.2: Upper cervical spinal cord lesion (see Fig. 8.21A).
Figure 17.3: Peripheral sensorimotor neuropathy (see Fig. 3.10).
Figure 17.4: Hemisection of the spinal cord (see Fig. 8.21E).
Figure 17.5: Myopathy (see Fig. 3.2).
Figure 17.6: Unilateral cerebral hemisphere lesion (see Fig. 13.19).
Figure 17.7: Myasthenia gravis (see Fig. 3.8).
Figure 17.8: Lower cervical spinal cord lesion (see Fig. 8.21B).
Figure 17.9: Spinal nerve root lesion (see Fig. 8.7).
Figure 17.10: Lumbar spinal cord lesion (see Fig. 8.21D).
Figure 17.11: Unilateral brain stem lesion (see Fig. 9.14).
Figure 17.12: Brachial plexus lesion (see Fig. 3.12).
Figure 17.13: Thoracic spinal cord lesion (see Fig. 8.21C).