To the Editor: Progressive supranuclear palsy is a movement disorder which often causes parkinsonian symptoms. Typical clinical findings in progressive supranuclear palsy are supranuclear vertical gaze palsy, postural instability, gait abnormality, bradykinesia, dysarthria, an increased axial tone, and a frightened facial expression. There are hints that patients diagnosed with progressive supranuclear palsy have an increased risk for developing depressive-like syndromes within the next years.1 However, to our knowledge, there is no data recording major depression as an antecedent symptom of later diagnosed progressive supranuclear palsy.
A 57-year-old man was admitted to our hospital for a major depressive syndrome without psychotic features. His main symptoms were depressed mood, anhedonia, apathy, loss of activity, difficulties in concentration, and self-reproach feelings. Attention and short-term memory were slightly impaired.
He indicated that this first depressive episode began 4 years earlier. No neurological, general medical, or psychiatric diseases had been described or diagnosed before. Within the first 3 months of the episode, depressive symptoms improved spontaneously; however, slightly depressed mood and concentration difficulties persisted until the time of admission. During the last year, decreased motor activity with slowed movements was observed. Moreover, he sometimes stumbled, had a tendency to fall backward, and had difficulties in walking down stairs. During the last month before admission these symptoms worsened. His wife described a change in his manner: he had become more and more apathetic, had increasing cognitive declines, and neared almost complete motor inactivity. He was admitted to our hospital for further diagnosis.
Neurological examination showed moderate hypomimia with a frightened facial expression, pathological eye movements with voluntary saccades, ocular pursuit movements, and vertical gaze palsy (impairment of voluntary vertical eye movements with preservation of reflex vertical eye movements). His motor activity was decreased; he had a slight rigor of the left arm and an increased axial tone with neck extension. Furthermore, we found a slight bradykinesia of the left arm and an unstable gait. He also described writing difficulties, but the type face was not changed in terms of a micrography.
No pathological findings were obtained by physical examination or standard laboratory tests including the liquor cerebrospinalis, EEG, ECG, and MRI of the head. To differentiate progressive supranuclear palsy from Parkinson’s disease and other related disorders, we tested the response to L-dopa. The intake of dopamine (Madopa® 500 mg/day) did not lead to any improvements. This lack of appreciable response to L-dopa and dopaminergic drugs characterizes progressive supranuclear palsy.
Taking all findings together, we diagnosed a progressive supranuclear palsy which started with a major depressive episode according to the DSM-IV criteria.
As far as we know, this case report is the first published report of a patient with a depressive episode as a first ("soft") sign of a progressive supranuclear palsy. There are reports and even studies of progressive supranuclear palsy-associated depressive-like symptoms, especially apathy, disinhibition, dysphoria, and anxiety.2 Awareness of possibly preceding psychiatric aspects like a depressive state as the first symptom of developing progressive supranuclear palsy may be helpful for an early diagnosis of this and other neurodegenerative diseases.