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Eating disorders are associated with various psychiatric and neurological diseases. Pathological eating behaviour ranges from reduced to excessive appetite, dysregulation of hunger and satiation signals, and odd food preferences. Hyperphagia and anorexia are reported in lesions (mostly tumours) involving the ventromedial hypothalamus.1 Moreover, eating disorders also occur in temporal lobe tumours, temporal lobe epilepsy, and advanced states of degenerative disease with neuronal loss in the medial temporal lobe. Hyperorality is part of the Kluver-Bucy syndrome which occurs in patients with bilateral mesial temporal lesions.1
We report a patient in whom compulsive hyperphagia was associated with a medial thalamic ischaemic stroke.
A 52 year old man complained of diplopia, dizziness, vertigo, decrease of consciousness, memory impairment, and hyperphagia. These symptoms occurred abruptly while he was painting the gate in his garden.
The diplopia and vertigo disappeared in about 15 minutes, while hyperphagia and memory impairment lasted for about 24 hours and completely disappeared the following day on awakening. Instead, amnesia concerning the event is still present.
The decrease of consciousness consisted of slight hypersomnolence (the patient could easily be awakened by auditory and verbal stimulation) and was present only at the onset, while memory impairment was noted only later. The patient’s wife reported that he kept repeating the same questions to her, and painted the garden gate incorrectly (using colours inappropriately). The patient was completely unaware of these symptoms, which were reported only by his wife.
Regarding the hyperphagia, his wife reported that the patient compulsively ate all the food he found in the refrigerator and in the kitchen. Apart from the fact that he was eating continuously all day long, when it was time for his lunch and evening meal, he always felt hungry and ready to eat, as his main concern was food, and his attention could not be diverted during his meals.
The following day his wife took him to the hospital. Neurological examination on admission revealed only retrograde amnesia about the events that had occurred in the previous 24 hours, along with fatuous behaviour. The medical history was not significant. Cranial computed tomography and extracranial Duplex ultrasonography were normal. Five days later, brain magnetic resonance imaging (MRI) revealed an ischaemic lesion involving the medial portion of the left thalamus in the territory of the tubero-thalamic perforating artery (fig 1). MRI-angiography of extracranial and intracranial cerebral arteries was normal.
A transthoracic echocardiogram was normal, while a transoesophageal echocardiogram revealed an atrial septal aneurysm without a patent foramen ovale. Conventional vascular risk factors (hypertension, diabetes, hypercholesterolaemia, and smoking) were absent. Routine laboratory studies including coagulation profiles were normal.
During the hospital admission, the patient’s clinical condition progressively improved and he was discharged eight days later without any neurological symptoms.
Two weeks later he was submitted to a neuropsychological test battery to assess reasoning (Raven PM47), short term memory (verbal and spatial span), learning (paired associate and Corsi spatial learning), attention (visual search), and frontal executive functions (Nelson card sorting test, trial making B, category, and literal fluency). Anxiety and depression were investigated by the state-trail anxiety inventory and the Beck depression inventory. Results were within the normal range (<1 SD) for all the tests.
The anatomical substrates of eating disorders are conventionally the basal ganglia and the cortico-limbic areas. In our patient compulsive hyperphagia was associated with the clinical features of medial thalamic ischaemia. The patient presented with signs and symptoms of the so called “top of the basilar syndrome” and of thalamic perforating artery infarction.
Thalamo-perforating arteries usually arise from the posterior cerebral artery and supply the posteromedial thalamus (PMT),2 which contains the rostral interstitial nucleus of the medial longitudinal fasciculus, the posterior inferior portion of the dorsomedial nucleus, the nucleus parafascicularis, the intralaminar nuclei, and sometimes the mamillothalamic tract. Unilateral infarcts of the PMT may cause a decrease in consciousness and neuropsychological disturbance (patients will be disoriented, unconcerned, apathetic, and may engage in behaviour involving the compulsive use of objects out of the behavioural context). A visual deficit (diplopia and vertical gaze functional impairment with up gaze palsy or combined up and down gaze palsy) are often reported because of the involvement of the upper mesencephalon.2 Neuropsychological disturbances are more marked and long lasting in patients with bilateral PMT infarction. Except for visual dysfunction, similar features are reported in anteromedial thalamic infarction.
In diencephalic lesions hyperphagia may result from hypothalamic, thalamo-cortical, or limbic dysfunction. Lesions involving the ventromesial hypothalamus, the amygdala, and the fibre bundle from the substantia nigra to the basal ganglia alter the signal of satiation and food intake.1 Eating disorders caused by hypothalamic dysfunction are characterised by dysregulation of hunger and satiation signals and are associated with other endocrine dysregulations.
Cortical lesions may cause eating disorders if they involve the temporal and frontal association areas connected to the basal and diencephalic systems. Moreover, clinical observations and animal studies suggest that the limbic structures and their connections are strongly involved in the regulation of appetite.3
In our patient the acute occurrence of compulsive eating was part of a complex behavioural and neuropsychological disturbance typical of medial thalamic dysfunction. Behavioural abnormalities may be more easily explained by bilateral involvement of the medial thalamic region. Indeed an embolic occlusion of the distal portion of the basilar artery may have caused a transient bilateral thalamic ischaemia. The definite infarct involved the left thalamus and was completely asymptomatic.
In our patient we believe that transient thalamo-cortical dysfunction because of impairment of the connection between the medial thalamic nuclei and the frontal or temporal lobes may have been the determinant of the compulsive hyperphagia. This compulsive hyperphagia may be the equivalent of the utilisation behaviour described in bilateral PMT infarction,4 in which patients automatically and inappropriately handle and use objects placed before them, even though told not use them.
Competing interests: none declared
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