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Factitious clock drawing and constructional apraxia
  1. I KHAN,
  2. I FAYAZ
  1. Division of Neurology
  2. Division of Neuropsychology
  3. Department of Medicine, Division of Neurology, The Toronto Hospital, University of Toronto, Toronto, ON, Canada
  1. Dr R Wennberg, EC8–022, The Toronto Hospital, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8. Telephone 001 416 603 5402; fax 001 416 603 5768.
  1. Division of Neurology
  2. Division of Neuropsychology
  3. Department of Medicine, Division of Neurology, The Toronto Hospital, University of Toronto, Toronto, ON, Canada
  1. Dr R Wennberg, EC8–022, The Toronto Hospital, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8. Telephone 001 416 603 5402; fax 001 416 603 5768.
  1. Division of Neurology
  2. Division of Neuropsychology
  3. Department of Medicine, Division of Neurology, The Toronto Hospital, University of Toronto, Toronto, ON, Canada
  1. Dr R Wennberg, EC8–022, The Toronto Hospital, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8. Telephone 001 416 603 5402; fax 001 416 603 5768.

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A 45 year old man presented with a 1 day history of headache, possible seizures, and left sided weakness. On the day of presentation the patient's wife had twice found him, inexplicably, on the floor. After the second such episode she brought him to hospital for evaluation. Examination disclosed a complete left hemiplegia and hemianaesthesia, although muscle tone was documented to be normal and the plantar responses downgoing bilaterally. Brain CT was normal and routine blood examination was unremarkable. There were no further seizure-like episodes and the patient was transferred to this hospital 10 days later, hemiplegia unchanged, for possible angiography and further investigations.

He was an exsmoker with hypercholesterolaemia and peripheral vascular disease which had been treated by a left femoral angioplasty 5 years earlier. The angioplasty was complicated by the occurrence of a seizure, thought to be related to dye injection, and phenytoin had been prescribed for a short time thereafter. There was a remote history of heavy alcohol use, but he had been abstinent for several years. His father had had a stroke at the age of 65.

Six months earlier the patient had also collapsed at home and been taken to hospital with a left hemiplegia. Brain CT at that time was normal, as were carotid Doppler studies and an echocardiogram. During that admission to hospital, several generalised seizure-like episodes were seen, some with retained consciousness, and he had again been started on phenytoin therapy. A follow up outpatient brain MRI was normal and it was concluded that the hemiplegia was non-organic in origin. He was described to have made a gradual, near complete, recovery from this first hemiplegic episode and was scheduled for an imminent return to work at the time of his relapse.

On transfer to this hospital the patient was alert, oriented, and cooperative. Although up to date on current affairs and able to describe the investigations performed at the transferring hospital, he scored only 23/30 on a mini mental state examination, with absent three word recall, impaired registration, and poor copying of a two dimensional line drawing. Further bedside neuropsychological testing showed other findings indicative of constructional apraxia and left hemineglect. Specifically, when asked to draw a clock with the time at 10 minutes to 2 o'clock, all the numbers, and the clockhands, were placed on the right hand side of the clock outline (figure A). Copying of three dimensional line drawings was also significantly impaired (figure B). When asked to bisect a line, however, the patient did so only minimally to the right of the midpoint (58% of the distance from the left side).

Cranial nerve examination suggested an incongruent and inconsistent left hemianopsia to confrontation testing but was otherwise normal, including bilaterally symmetric optokinetic nystagmus. Motor examination showed paralysis of the left arm and leg, with bilaterally symmetric bulk, tone, and deep tendon reflexes. The plantar response was flexor bilaterally. Sensory examination showed decreased pinprick and absent light touch, joint position sense, and vibration sense on the entire left side. There was also impaired perception of a tuning fork's vibration on the left side of the forehead, with a distinct demarcation in the midline. The rest of the physical examination was unremarkable.

Brain CT and MRI, CSF examination, and routine EEG were normal. Routine haematological and metabolic analyses plus erythrocyte sedimentation rate, serum lactate, prothrombin time/partial thromboplastin time, fasting serum glucose, HbA1c, serum Ig survey, and thyroid stimulating hormone were all within normal limits. A hypercoagulability profile was negative. A lipid profile showed mild hyperlipidaemia with increased low density lipoprotein (3.92 mmol/l) and triglycerides (4.30 mmol/l) and low high density lipoprotein (0.73 mmol/l). Serum phenytoin concentration was therapeutic at 74 μmol/l. An ECG was normal.

(A) Asked to: “put all the numbers on a clock and make the time ten to two”. (B) Patient's copies (at right) of three dimensional line drawings. Top: common constructional distortion of cube. Bottom: unusual mirror image representation of house.

Ophthalmological consultation and formal visual field testing demonstrated a concentrically constricted field of mild degree in the right eye and tunnel vision in the left eye.

The patient consented to overnight video-EEG monitoring and was seen on multiple occasions to move his left arm and/or leg in a normal fashion, at one point using the left arm to readjust his bed covers shortly after arousal from sleep, before glancing briefly at the video camera and completing the task with his right arm. The prolonged EEG was normal.

A formal neuropsychological assessment performed in hospital documented impaired attention, concentration, and working memory, as well as several atypical calculation and spelling errors, the second involving unusual “near miss” letter substitutions or reversals (for example, “anixety”, “excecutive”). The formal testing identified no consistent evidence of visuospatial deficits or constructional apraxia. The findings were interpreted as inconsistent with the patient's history but the possibility of a factitious aetiology was not specifically addressed—that is, tests designed to detect malingering during neuropsychological testing1 2 were not administered by the examiner, who had not been informed at the time of consultation of the presumptive neurological diagnosis of malingering or factitious disorder.

No further investigations were performed and the patient was transferred via the original hospital to a rehabilitation facility and subsequently discharged to home. Confronted with the findings of the video monitoring the patient appeared sanguine and accepting of the evidence that he should be able to move his left side. Six months later he was ambulatory but otherwise not significantly improved. He had been assessed by a psychiatrist but had refused psychiatric follow up, electing instead to be followed up by a psychologist. He understood his diagnosis to be “conversion disorder” and reported that he was actively collecting information on the subject via the internet.

Outpatient brain SPECT and visual and somatosensory evoked potentials performed 1 year after discharge demonstrated no hemispheric abnormalities. The patient remained off work and was receiving disability funding. He walked with a limp favouring his left side and complained of persistent decreased sensation on the left side. Forced choice sensory testing of finger and arm movement on the left3 demonstrated performance to be worse than chance (68% wrong choices). Motor bulk, tone, and reflexes were symmetric and plantar responses downgoing. He drew a clock normally at the 1 year follow up.

The clinical and laboratory findings described above indicate beyond any doubt the non-organic nature of this patient's left hemiplegia/hemianaesthesia. His seizure-like episodes at presentation are presumed to have been non-epileptic in origin (as had been suspected during his previous admission to hospital) although this cannot be definitively proved.

The inability to copy line drawings or to draw a clock is, from a neurologist's perspective, typically associated with parietal lobe dysfunction, usually of the non-dominant hemisphere, especially if associated with left hemispatial neglect.4 To our knowledge, this is the first reported case of factitious clock drawing and constructional apraxia. Bedside mental status testing also demonstrated the more common simulated deficits of impaired attention and absent three word recall.1 In retrospect, the severe neglect on clock drawing was perhaps “too good to be true”, especially in the light of the near normal line bisection demonstrated on the same day. The mirror image distortion of the house was also very unusual and, furthermore, the mirror reversal itself is evidence of lack of clinical neglect. The distortion of the cube, however, could easily be misinterpreted as evidence of organic constructional impairment if seen in the absence of the other relevent clinical and laboratory information.

During follow up, the patient admitted to feeling tremendous occupation related stresses, and described how he had come to both fear and detest his job. Given the clear benefit to the patient of removal from his work environment, the relapse of his symptomatology just as he was scheduled for return to work after his first non-organic hemiplegic episode, and the intentionality required to feign poor clock drawing and constructional apraxia, there is much to support a diagnosis of malingering.5 Nevertheless, classification as a factitious disorder is at least as justifiable in view of the patient's willingness to undergo medical investigations, including video monitoring.

It is unclear how or when the patient acquired the information needed to mimic a constructional apraxia. Previous bedside neuropsychological evaluations may have served to familiarise him with the format of such testing, acting as an impetus to research the issue of stroke and focal brain deficits (which might also have occurred after his father's stroke), much in the same way he is now researching conversion disorder, thereby discovering what expected answers should look like. Despite repeated questioning, however, no evidence could be gathered from the patient to support this speculation.


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