Color Atlas of Neurology

Memory

Memory involves the acquisition, storage, recall, and reproduction of information. Memory depends on intact functioning of the limbic system (p. 144) and areas of the brain that are connected to it.

Declarative or explicit memory (i.e., memory for facts and events) can be consciously accessed and depends on intact functioning of the mediobasal portion of the temporal lobe. The duration of information storage may be relatively short (short-term, immediate, and working memory) or long (long-term memory). Verbal (telephone number) or visuospatial information (how to find a street) can be directly recalled from shortterm memory. The entorhinal cortex plays a key role in these memory functions: all information from cortical regions (frontal, temporal, parietal) travels first to the entorhinal cortex and then, by way of the parahippocampal and perirhinal cortex, to the hippocampus. There is also a reciprocal projection from the hippocampus back to the entorhinal cortex. Long-term memory stores events of personal history that occurred at particular times (episodic memory for a conversation, one’s wedding day, last year’s holiday; orbitofrontal cortex) as well as conceptual, non–time-related knowledge (semantic memory for the capital of Spain, the number of centimeters in a meter, the meaning of the word “stethoscope”; subserved by different cortical regions).

Nondeclarative (procedural, implicit) memory, on the other hand, cannot be consciously accessed. Learned motor programs (riding a bicycle, swimming, playing the piano), problem-solving (rules), recognition of information acquired earlier (priming), and conditioned learning (avoiding a hot burner on the stove, sitting still in school) belong to this category. Nondeclarative memory is mediated by the basal ganglia (motor function), neocortex (priming), cerebellum (conditioning), striatum (agility), amygdala (emotional responses), and reflex pathways.

Examination. Only disturbances of declarative memory (amnesia) can be studied by clinical examination. Short-term memory: the acquisition of new information is tested by having the patient repeat a series of numbers or groups of words and asking for this information again

5–10 minutes later. The patient’s orientation (name, place of residence/address, time/date) and long-term memory (place of birth, education, place of employment, family, general knowledge) are also tested by directed questioning.

Memory Disorders (Amnesia)

Forgetfulness. Verbal memory does not decline until approximately age 60, and even then only gradually, if at all. Aging is, however, often accompanied by an evident decline in information processing ability and attention span (benign senescent forgetfulness). These changes occur normally, yet to a degree that varies highly among individuals, and they are often barely measurable. They are far less severe than fullblown dementia, but they may be difficult to distinguish from incipient dementia.

Amnesia. Anterograde amnesia is the inability to acquire (declarative) information, for later recall, from a particular moment onward; retrograde amnesia is the inability to remember (declarative) information acquired before a particular moment (p. 269). Amnestic patients commonly confabulate (i.e., fill in gaps in memory with fabricated, often implausible information); they may be disoriented and lack awareness of their own memory disorder. For individual symptoms and their causes, see Table 13 (p. 365).

Dementia is a newly occurring, persistent, and progressive loss of cognitive function. Both short-term and long-term memory are impaired, in conjunction with at least one of the following disorders: aphasia, apraxia, agnosia, or impairment of abstract thinking, decisionmaking ability, visuospatial performance, planned action, or personality. Professional, social and interpersonal relationships deteriorate, and the sufferer finds it increasingly difficult to cope with everyday life without help. The diagnosis of dementia requires the exclusion of disturbances of consciousness (e. g., delirium) and of psychiatric disease (e. g., depression, schizophrenia). The differential diagnosis also includes benign senescent forgetfulness (“normal aging,” in which daily functioning is unimpaired) and amnestic disorders. Approximately 90% of all cases of dementia are caused by Alzheimer disease (p. 297) or cerebrovascular disorders; diverse etiologies account for the rest. The physician confronted with a case of incipient dementia must distinguish primary dementia from that secondary to another disease (Table 14, p. 366). The objective is early determination of the etiology of dementia, especially when these are treatable or reversible.

Examination. The patient or another informant should be asked for an account of the duration, type, and extent of problems that arise in every-

day life. The clinical examination is used to ascertain the type and severity of cognitive deficits and any potential underlying disease. Standardized examining instruments are useful for precise documentation and differentiation of the cognitive deficits. Rapid tests for dementia, such as the Mini-Mental Status Examination, mini-syndrome test, and clock/numbers test, are useful for screening. Function-specific neurophysiological tests permit diagnostic assessment of individual aspects of cognition including orientation, attention, concentration, memory, speech, and visual constructive performance. Laboratory tests (ESR1, differential blood count, electrolytes, liver function tests, BUN2, creatinine, glucose, vitamin B12, folic acid, TPHA3, TSH4, and HIV5), EEG, and diagnostic imaging techniques (CT6, MRI7, SPECT8, and PET9) provide further useful information for classification and determination of the cause of dementia. None of these diagnostic techniques alone can pinpoint the etiology of dementia; definitive diagnosis practically always requires multiple tests and examinations. Diagnostic imaging is of particular importance in patients with the subacute onset of cognitive impairment or amnesia (!1 month), fluctuation or acute worsening of symptoms, papilledema, visual field defects, headaches, a recent head injury, known malignancies, epilepsy, a history of stroke, urinary incontinence, or an abnormal gait.

The autonomic nervous system (ANS) is so called because its functions are normally not subject to direct voluntary control. It regulates hormonal and immunological processes as well as the functioning of major organ systems (cardiovascular, respiratory, gastrointestinal, urinary, and reproductive systems).

ANS, Central Portion

Central components of the ANS are found in the cerebral cortex (insular, entorhinal, orbitofrontal, and frontotemporal areas), the hypothalamus, the limbic system, the mid brain (periaqueductal gray substance), the medulla (nucleus of the solitary tract, ventrolateral and ventromedial areas of the medulla), and the spinal cord (various tracts and nuclei, discussed in further detail below).

Afferent connections. Afferent impulses enter the ANS from spinal tracts (anterolateral fasciculus = spinothalamic + spinocerebellar + spinoreticular tracts), brain stem tracts (arising in the reticular formation), and corticothalamic tracts, and from the circumventricular organs. The latter are small clusters of specialized neurons, lying on the surface of the ventricular system, that sense changes in the chemical composition of the blood and the cerebrospinal fluid (i.e., on both sides of the blood–CSF barrier). These organs include the organum vasculosum of the lamina terminalis (in the roof of the third ventricle behind the optic chiasm cytokines/ fever), the subfornical organ (under the fornices between the foramina of Monro angiotensin II/blood pressure and fluid balance), and the area postrema (rostral to the obex on each side of the fourth ventricle cholecystokinin/ gastrointestinal function, food intake).

Efferent connections. Projections from the hypothalamus and brain stem, particularly from the brain stem reticular formation, travel to the lateral horn of the thoracolumbar spinal cord, where they form synapses onto the sympathetic neurons of the spinal cord. The latter, in turn, project preganglionic fibers to the sympathetic ganglia (p. 147). The parasympathetic neurons receive input from higher centers in similar fashion and project in turn to parasympathetic ganglia that are generally located near the end organs they serve. The hypothalamus regulates hormonal function through its regulator hormones as well as efferent neural impulses.

Neurotransmitters. The main excitatory neurotransmitter is glutamate, and the main inhibitory neurotransmitter is γ-aminobutyric acid (GABA). Modulating neurotransmitters include acetylcholine, amines, neuropeptides, purines, and nitric oxide (NO).

ANS, Peripheral Portion (p. 146)

The sympathetic and parasympathetic components are both structurally and functionally segregated.

Spinal nuclei. Sympathetic spinal neurons lie in the lateral horn (intermediolateral and intermediomedial cell columns) of the thoracolumbar spinal cord (T1–L2) and are collectively termed the thoracolumbar system. Parasympathetic spinal neurons lie in the brain stem (with projections along CN III, VII, IX, X) and the sacral spinal cord (S2–S4), and are collectively termed the craniosacral system. The intestine has its own autonomic ganglia, which are located in the myenteric and submucous plexuses (p. 154).

Afferent connections. Afferent impulses to the ANS enter the spinal cord via the dorsal roots, and the brain stem via CN III, VII, IX and X.

Efferent connections. The projecting fibers of the spinal autonomic neurons (preganglionic fibers) exit the spinal cord in the ventral roots and travel to the paravertebral and prevertebral ganglia, where they synapse onto the next neuron of the pathway. The sympathetic preganglionic fibers (unmyelinated; white ramus communicans) travel a short distance to the paravertebral sympathetic chain, and the postganglionic fibers (unmyelinated; gray ramus communicans) travel a relatively long distance to the effector organs. An exception to this rule is the adrenal medulla: playing, as it were, the role of a sympathetic chain ganglion, it receives long preganglionic fibers and then, instead of giving off postganglionic fibers, secretes epinephrine into the bloodstream. The parasympathetic preganglionic fibers are long; they project to ganglia near the effector organs, which, in turn, give off short postganglionic processes.

Neurotransmitters. Acetylcholine is the neurotransmitter in the sympathetic and parasympathetic ganglia. The neurotransmitters of the postganglionic fibers are norepineprhrine (sympathetic) and acetylcholine (parasympathetic). Neuromodulators include neuropeptides (substance P, somatostatin, vasoactive intestinal