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Figure 25-2 Schematic block diagram of the limbic connections The internal connections (bold lines) represents the circuit described by Papez The external connections (thin lines) are more recently described pathways This gure also shows the connections to the amygdala and prefrontal and association cortices (Reproduced with permission from Kandel ER, Schwartz JH, Jessell TM: Principles of Neural Science, 4th ed New York, McGraw-Hill, 2000)

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expression The intermediate position of the limbic structures enables them to transmit neocortical effects from their outer side to the hypothalamus and midbrain on their inner side The role of the cingulate gyrus in the behavior of animals and humans has been the subject of much discussion Stimulation is said to produce autonomic effects similar to the vegetative correlates of emotion (increase in heart rate and blood pressure, dilatation of pupils, piloerection, respiratory arrest, breath-holding) More complex responses such as fear, anxiety, or pleasure have been reported during neurosurgical stimulative and ablative procedures, although these results are inconsistent Bilateral cingulectomies performed in psychotic and neurotic patients result in an overall diminution of emotional reactions (Ballantine et al; Brown) Some investigators believe that the cingulate gyri are also involved in memory processing (functioning presumably in connection with the mediodorsal thalamic nuclei and mediotemporal lobes) and in exploratory behavior and visually focused attention In humans, this system appears to be more ef cient in the nondominant hemisphere, according to Bear Baleydier and Mauguiere emphasize this dual function in cognition and in emotional reactions of the cingulate gyrus Another aspect of limbic function has come to light as information is being acquired about neurotransmitters The concentration of norepinephrine is highest in the hypothalamus and next highest in the medial parts of the limbic system; at least 70 percent of this monoamine is concentrated in terminals of axons that arise in the medulla and in the locus ceruleus of the rostral pons Axons of other ascending bers especially those originating in the reticular formation of the midbrain and terminating in the amygdala and septal nuclei as well as in lateral parts of the limbic lobe are rich in serotonin The axons of neurons in the ventral tegmental parts of the midbrain, which ascend in the medial forebrain bundle and the nigrostriatal pathway, contain a high content of dopamine.

These are best portrayed by the patient with a orid delirium Threatened by imaginary gures and voices that seem real and Table 25-1 Neurology of emotional disturbances I Disturbances of emotionality due to: A Perceptual abnormalities (illusions and hallucinations) B Cognitive derangements (delusions) II Disinhibition of emotional expression A Emotional lability B Pathologic laughing and crying III Rage reactions and aggressivity IV Apathy and placidity A Kluver-Bucy syndrome B Other syndromes (frontal and thalamic) V Altered sexuality VI Endogenous fear, anxiety, depression, and euphoria

inescapable, the patient trembles, struggles to escape, and displays the full picture of terror The patient s affect, emotional reaction, and visceral and somatic motor responses are altogether appropriate to the content of the hallucinations We have seen a patient slash his wrists and another try to drown himself in response to hallucinatory voices that admonished them for their worthlessness and the shame they had brought on their families But the abnormality in these circumstances is one of disordered perception and thinking, and we have no reason to believe that there is a derangement of the mechanisms for emotional expression There also occurs a state dif cult to classify of overwhelming emotionality in patients who are in severe acute pain The patient s attention can be captured only brie y, but within moments there is a return to an extreme state of angst, groaning, and anger We have encountered this with spinal subdural hemorrhage, subarachnoid hemorrhage, explosive migraine, trauma with multiple fractures, and intense pelvic, renal, or abdominal pain, all understandable as responses to extralimbic stimuli

Table 25-2 Causes of pseudobulbar affective display Bilateral strokes (lacunes in the cerebral hemispheres or pons most often, and after several strokes in succession) Binswanger diffuse leukoencephalopathy (Chap 34) Amyotrophic lateral scerlosis with pseudobulbar palsy Progressive supranuclear palsy Multiple sclerosis with bilateral corticobulbar demyelinative lesions Bilateral traumatic lesions of the hemispheres Hypoxic-ischemic encephalopathy Pontine myelinolysis Wilson disease

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