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Lyme Neuroborreliosis Dismissed as Psychosomatic: The Diagnosis Came After 17 kg of Weight Loss

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A previously healthy 30-year-old man developed severe headaches, neck pain, dizziness, sensitivity to light, nausea, vomiting and overwhelming fatigue. Within six weeks, he had lost 11 kg and was sleeping as much as 16 hours a day. His symptoms were getting progressively worse, yet neurological examinations, routine blood tests and brain imaging failed to identify a cause. A psychiatric assessment also found no abnormalities, and depression was excluded. Nevertheless, he was discharged from hospital with a diagnosis of chronic tension headache and psychosomatic complaints.

The case, published in BMJ Case Reports in 2012 under the title Misleading presentation of acute Lyme neuroborreliosis, illustrates how a serious neurological infection can remain undetected when its presentation does not fit the expected clinical picture. More importantly, it documents how unexplained symptoms were initially attributed to psychosomatic causes before an important investigation had been performed.


When Normal Tests Became a Psychosomatic Explanation

During his first hospital admission, the patient underwent extensive neurological and psychiatric assessments. CT and contrast-enhanced MRI examinations of his brain and neck showed no abnormalities. Routine biochemical investigations were normal, and neurological examination was largely unremarkable apart from a slight disturbance in his gait. There was no muscle weakness, sensory loss or other obvious neurological deficit to explain the severity of his illness.

With no explanation emerging from these investigations, clinicians considered his symptoms psychosomatic. He was discharged despite having experienced substantial weight loss, extreme fatigue and symptoms severe enough to interfere with normal daily life. Crucially, no lumbar puncture had been performed.

Two weeks later, he returned to hospital in a considerably worse condition. His total weight loss had reached 17 kg, and he had been unable to work for a month. Further investigations, including abdominal ultrasound and gastroscopy, again failed to identify an explanation. The absence of abnormalities on routine testing had not made the underlying disease disappear.

A more detailed medical history finally revealed something important: the patient regularly walked in forests. Although he had never noticed the characteristic expanding rash associated with Lyme disease, his possible exposure to infected ticks prompted clinicians to investigate Borrelia infection.


The Investigation That Changed Everything


Blood testing detected antibodies against Borrelia burgdorferi. A subsequent lumbar puncture revealed markedly abnormal cerebrospinal fluid, including an opening pressure of 50 cm H2O, a white blood cell count of 1,221 cells/µL, protein of 354 mg/dL and glucose of 1.7 mmol/L. Additional testing demonstrated intrathecal production of Borrelia-specific antibodies, establishing the diagnosis of acute Lyme neuroborreliosis.

These were not subtle findings. The cerebrospinal fluid demonstrated substantial inflammation involving the central nervous system, despite the earlier normal brain imaging, routine blood investigations and largely normal neurological examination. The authors acknowledged that lumbar puncture should, in retrospect, have been performed during the initial admission.

"This case emphasises the importance of complete history taking, since the clue to correct diagnosis was hidden within the fact that the patient had been hiking in the forest."

Winter EM, Rothbarth PH and Delfos NM, BMJ Case Reports, 2012.

The patient received intravenous ceftriaxone at 2 g daily for 14 days. His symptoms began improving within days, his body weight returned to normal within a month, and he was able to resume work almost immediately. At six-month follow-up, he remained healthy without recurrence of his complaints.


The Problem With Premature Psychosomatic Attribution

One particularly relevant detail is the differential diagnosis documented by the authors. Alongside neurological, infectious, endocrine and gastrointestinal conditions, clinicians considered depression, stress-related psychosomatic complaints and conversion disorder. The patient was not formally diagnosed with Functional Neurological Disorder (FND), but conversion disorder was explicitly among the possibilities considered, and psychosomatic complaints formed part of his initial discharge diagnosis.

That distinction is important. This is not a documented case of FND being overturned by a Lyme diagnosis. It is a documented case of a serious neurological infection initially being interpreted as psychosomatic because conventional investigations had not revealed its cause.

The authors described the presentation as highly unusual because the patient lacked the characteristic findings commonly associated with Lyme neuroborreliosis. He had no documented facial paralysis, painful radiculitis or obvious neurological deficits. His MRI was normal, his routine blood tests offered little assistance, and his symptoms were predominantly nonspecific. Yet the eventual diagnosis was supported by substantial cerebrospinal fluid abnormalities and Borrelia-specific antibody production within the central nervous system.

There is an obvious diagnostic lesson here. A normal MRI does not establish that symptoms are functional or psychological. Neither does an unrevealing routine blood panel or the absence of obvious weakness on examination. Those findings establish the limits of the investigations performed, not the absence of disease. In this case, the missing evidence was obtained only after the patient's condition had deteriorated further.

The patient's progressive weight loss, persistent headaches, nausea, extreme fatigue and functional deterioration were not explained by the initial diagnosis. The authors themselves recognised that the lumbar puncture should have been performed earlier. The problem was therefore not simply that Lyme neuroborreliosis presented atypically, but that a psychosomatic explanation was accepted before the investigation that ultimately established the diagnosis.

This single case does not establish how frequently Lyme neuroborreliosis is mistaken for psychosomatic illness, nor does it suggest that every patient with unexplained neurological symptoms requires Lyme testing. It does, however, provide a concrete example of why exposure history, symptom progression and reconsideration of an initial diagnosis matter, particularly when the patient continues to deteriorate.

The man did not develop a neurological infection after being labelled psychosomatic. He already had one. The diagnosis changed when clinicians obtained the evidence that had been missing.


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