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Anorexia nervosa remission following left thalamic stroke
  1. H Dusoir1,
  2. C Owens2,
  3. R B Forbes2,
  4. J I Morrow2,
  5. P A Flynn3,
  6. M O McCarron4
  1. 1Department of Neuropsychology, Royal Victoria Hospital, Belfast, BT12 6BA, UK
  2. 2Department of Neurology, Royal Victoria Hospital, Belfast, BT12 6BA, UK
  3. 3Department of Neuroradiology, Royal Victoria Hospital, Belfast, BT12 6BA, UK
  4. 4Department of Neurology, Altnagelvin Hospital, Londonderry, BT47 6SB, UK
  1. Correspondence to:
 Dr M McCarron
 Department of Neurology, Altnagelvin Hospital, Londonderry, BT47 6SB, UK;

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Anorexia nervosa is an intense fear of weight gain, inaccurate perception of body size, weight or shape, amenorrhoea, and a body weight <85% of expected weight (or body mass index (BMI) ⩽17.5). We report a patient who, following a left thalamic stroke demonstrated a remarkable recovery from a 7 year history of anorexia nervosa.

The patient grew up in a family with both parents and two older brothers. When she was 14 years old, a young cousin died of a “brain haemorrhage”. Six months later the patient started a “healthy eating” regimen. She was first admitted to hospital for her eating disorder in April 1995, aged 15 years, and was prescribed antidepressant medication. The problem continued despite psychiatric and psychological treatment (usual weight 43 kg, BMI 17).

In May 2002, aged 22 years, she experienced a sudden onset of right arm and leg weakness with a sensory disturbance of the right face, arm, and leg. There was no history of diabetes, cigarette smoking, illicit drugs, or oral contraceptive use. She was admitted to hospital. She was told that a computerised tomogram (CT) showed that she either had a brain tumour or had suffered a stroke. She was transferred to the regional neurology unit. There she was alert, but had a slight decrease in sensation on the right side of the face; there was no visual field defect. She had a right pronator drift. She had grade 4 strength throughout the right upper limb. Leg strength was normal. The right arm and leg were mildly hyperaesthetic and there was impaired proprioception in the right fingers. There was right sided ataxia. On the right she had brisk reflexes and an extensor plantar response.

Her brain CT demonstrated left thalamic hypoattenuation, which on magnetic resonance imaging showed involvement of the left posterolateral thalamus and posterior temporal lobe (fig 1). The infarct area involved the left inferolateral artery territory. Magnetic resonance angiography was normal. Other investigations (chest x ray, electrocardiogram, thoracic echocariogram, full blood profile, thrombophilia screen, glucose, liver function tests, and thyroid function tests) were normal. The patient was extremely anxious and thought frequently about her cousin’s death. However, she gradually improved and reported to a neuropsychologist that she no longer had an eating disorder. Her realisation came quite suddenly 3 days after her transfer to the neurology service. She chose cauliflower cheese for her evening meal and asked a visitor for a chocolate chip biscuit; neither of these foods would have been acceptable as part of her anorexic diet.

Figure 1

 Axial T2 magnetic resonance images demonstrating high signal and mild mass effect in the posterolateral thalamus and posteromedial temporal lobe consistent with recent infarction. The infarct distribution corresponds to thalamogeniculate branches of the posterior cerebral artery.

Within 6 months the patient gained 4 kg in weight (41 kg to 45 kg, BMI 18.7). Regular menses returned after two years of amenorrhoea. Eight months after the stroke she wrote the following descriptions of her feelings before and after her stroke: Pre-stroke: “Anorexia controlled my life and influenced things which I did or did not do.” “… relationships – lost interest in them. Only interested in anorexia.”

Of her post-stroke state she said, “I have no feelings of guilt. I no longer count calories. I am relaxed about eating/around food. I can eat out in restaurants now.”

She continued with antidepressant medication and her mood remained stable. The patient completed the Eating Disorders Inventory-21 from the perspectives of pre-stroke and 13 months post-stroke. The bulimia and interpersonal trust scales were at the mean for non-patient college females both pre- and post-stroke. Drive for thinness and body dissatisfaction were high pre-stroke, even in comparison with the eating disorder group. The scores on drive for thinness, body dissatisfaction, ineffectiveness, and interoceptive awareness all fell dramatically post-stroke, and her post-stroke scores were close to the mean for non-patient college females.


Our patient demonstrated sustained remission from anorexia nervosa for a 13 month period following a left posterolateral thalamic stroke. She reported significantly changed attitudes to food. Clearly the pre-stroke assessment, completed retrospectively, has to be interpreted cautiously. Nevertheless, the findings strongly suggest important shifts in her attitudes. There are two possible hypotheses to account for her anorexia remission: (a) the cerebral infarct switched off her anorexia; or (b) the personal trauma of the stroke, including being told that she might have a brain tumour or had had a stroke.

Thalamic pathways have been implicated in the control of normal eating. As part of Papez circuit, the anterior thalamus projects to the cingulate gyrus and the dorsomedial thalamus projects to the basal nuclei of Meynert. The thalamus may have an integrative role with higher order somatosensory and visuospatial function. Neuroimaging techniques have demonstrated several abnormalities in the anorectic state, some of which are reversible with treatment. The smaller size of the thalamus2 and thalamic perfusion changes in anorexics3 suggest that the thalamus plays an important role in anorexia nervosa. Our patient demonstrated the usual clinical features of lateral thalamic infarction: hemiataxia, and hemisensory and motor deficit.

Hyperphagia has been reported with a variety of lesions in the thalamus, hypothalamus and frontal lobe. Lesions in these areas have also been implicated in the onset of anorexia nervosa. In contrast to our patient’s remission from anorexia with a left posterolateral thalamic infarct, anorexia has been associated with dorsomedial thalamic infarction. Stereotactic thalamotomy has been used as a treatment of anorexia nervosa.4,5The right dorsomedial and intralaminar thalamic nuclei were lesioned in one patient,4 while a bilateral procedure was performed in two;5 all three made a sustained improvement. There are other reports of improvements following an encephalitic illness and a right thalamic haemorrhage.

Trauma may contribute to the development of anorexia nervosa. However, there are no reports, to our knowledge, of a traumatic event leading directly to the cessation of an eating disorder. Our patient was traumatised by the sudden death of a 21 year old cousin from a “brain haemorrhage” when she was aged 13 years. A change in her eating pattern developed into anorexia nervosa over subsequent months.

Whether this sudden and sustained recovery from an eating disorder was due to a psychologically traumatic event or to the direct effect of the left thalamic stroke is not certain. The abruptness of the change, and reported functional thalamic abnormalities in anorectics that reverse in remission, lends weight to the latter hypothesis.



  • Competing interests: none declared