Autonomic
Nervous System
Anatomy of the autonomic nervous system
The autonomic nervous system (ANS) includes those nerve
cells and fibres that innervate internal and glandular organs. They subserve
the regulation of processes that usually are not under voluntary influence.
•
The efferent conducting pathway from the
central nervous system (CNS) to the innervated organ always consists of two
succeeding neurones: a preganglionic and a postganglionic, with
the former having its cell body in the CNS (see Chapter 2).
•
The ANS is subdivided into the enteric, sympathetic
and parasympathetic nervous systems – the latter two commonly exert
opposing influences on the structure they are innervating.
•
The sympathetic nervous system preganglionic
neurones are found in the intermediate part (lateral horn) of the spinal
cord from the upper thoracic to mid-lumbar cord (T1–L3).
•
The preganglionic parasympathetic neurones have
their cell bodies in the brainstem and sacrum.
•
The postganglionic cell bodies are found in the
vertebral and prevertebral ganglia in the sympathetic nervous system but in the
parasympathetic system they are situated either adjacent to or in the walls of
the organ they supply.
•
In addition to anatomical differences the
sympathetic nervous system uses noradrenaline (norepinephrine; NA) as
its postganglionic transmitter while the parasympathetic nervous system uses acetylcholine
(ACh). Both systems use ACh at the level of the ganglia.
Central nervous system control of the autonomic nervous system
The CNS control of the ANS is complex, involving a number of
brainstem structures as well as the hypothalamus (see Chapter 11). The
main hypothalamic areas involved in the control of the ANS are the ventromedial
hypothalamic area in the case of the sympa- thetic nervous system and the lateral
hypothalamic area in the case of the parasympathetic nervous system.
Controlling pathways are direct or indirect via a number of brainstem
structures such as the periaqueductal grey matter and parts of the reticular
formation (see Chapter 8).
Clinical features of damage to the autonomic nervous system
Damage to the ANS can either be local to a given anatomical
structure, or generalized when there is loss of the whole system caused by
either a central or peripheral disease process.
•
Focal peripheral lesions: These are not
uncommon and the deficiencies resulting from these lesions can be easily
predicted. For example, loss of the sympathetic innervation to the eye results
in pupillary constriction (miosis), drooping of the upper eyelid (ptosis) and
loss of sweating around the eye (anhydrosis) – a triad of signs known as Horner’s
syndrome. Other examples include the reflex sympathetic dystrophies
where there is severe pain and auto- nomic changes confined to a single
limb, often in response to some trivial injury. The exact role of the
sympathetic nervous system in the genesis of these conditions is not known, as
local sympathectomies are not always effective treatments. However, in some
instances these treatments can help which may relate to the fact that the
nociceptors can start expressing receptors for NA (see Chapters 32 and 33).
•
More global damage to the ANS: This can
occur because of degeneration of the central neurones either in isolation (e.g.
pure autonomic failure) or as part of a more widespread
degenerative process as is seen, for example, in multiple-system atrophy,
where there may be additional cell loss in the basal ganglia and cerebel- lum.
Alternatively, the autonomic failure may result from a loss of the peripheral
neurones, e.g. in diabetes mellitus, certain forms of amyloidosis, alcoholism
and Guillain–Barré syndrome. Finally, abnormalities in the ANS
can be seen with certain toxins (e.g. botulism; see Chapter 16) as well as in Lambert–Eaton
myasthenic syndrome (see Chapters 16 and 62).
In all these cases the patient presents with orthostatic and
post-prandial hypotension (syncopal or presyncopal symptoms on standing,
exercising or eating a big meal) with a loss of variation in heart rate, bowel
and bladder disturbances (urinary urgency, frequency and incontinence),
impotence, loss of sweating and pupillary responses. The symptoms are often
difficult to treat and a number of agents are used to try to improve the
postural hypotension and sphincter abnormalities. Agents for postural hypotension
include fludrocortisone, ephedrine, domperidone, midodrine and vasopressin
analogues (all of which cause fluid retention).
