Does the representation of time depend on the cerebellum? Effect of cerebellar stroke

Authors:

• Deborah L. Harrington

• Roland R. Lee

• Lara A. Boyd

• Steven Z. Rapcsak

• Robert T. Knight

Date: 2004

PubMed: 14711883

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Abstract:

Behaviours that appear to depend on processing temporal information are frequently disrupted after cerebellar damage. The present study examined the role of the cerebellum in explicit timing and its relationship to other psychological processes. We hypothesized that if the cerebellum regulates timekeeping operations then cerebellar damage should disrupt the perception and the reproduction of intervals, since both are thought to be supported by a common timekeeper mechanism. Twenty-one patients with cerebellar damage from stroke and 30 normal controls performed time perception and time reproduction tasks. In the time reproduction task, timing variability was decomposed into a central timing component (clock variability) and a motor component (motor implementation variability). We found impairments only in time reproduction (increased clock variability) in patients with medial and lateral damage involving the middle- to superior-cerebellar lobules. To explore potential reasons for the temporal processing deficits, time reproduction and perception performance were correlated with independent measures of attention, working memory, sensory discrimination and processing speed. Poorer working memory correlated with increased variability in the 'clock' component of time reproduction. In contrast, processing speed correlated best with time perception. The results did not support a role for the cerebellum in timekeeping operations. Rather, deficits in timing movements may be related to a disruption in acquiring sensory and cognitive information relevant to the task, coupled with an additional impairment in the motor-output system.

Neural representations of skilled movement

Authors:

• Kathleen Y. Haaland

• Deborah L. Harrington

• Robert T. Knight

Date: 2000

PubMed: 11050030

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Abstract:

The frontal and parietal cortex are intimately involved in the representation of goal-directed movements, but the crucial neuroanatomical sites are not well established in humans. In order to identify these sites more precisely, we studied stroke patients who had the classic syndrome of ideomotor limb apraxia, which disrupts goal-directed movements, such as writing or brushing teeth. Patients with and without limb apraxia were identified by assessing errors imitating gestures and specifying a cut-off for apraxia relative to a normal control group. We then used MRI or CT for lesion localization and compared areas of overlap in those patients with and without limb apraxia. Patients with ideomotor limb apraxia had damage lateralized to a left hemispheric network involving the middle frontal gyrus and intraparietal sulcus region. Thus, the results revealed that discrete areas in the left hemisphere of humans are critical for control of complex goal-directed movements.

Spatial deficits in ideomotor limb apraxia: a kinematic analysis of aiming movements

Authors:

• Kathleen Y. Haaland

• Deborah L. Harrington

• Robert T. Knight

Date: 1999

PubMed: 10356068

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Abstract:

Ideomotor limb apraxia is a classic neurological disorder manifesting as a breakdown in co-ordinated limb control with spatiotemporal deficits. We employed kinematic analyses of simple aiming movements in left hemisphere- damaged patients with and without limb apraxia and a normal control group to examine preprogramming and response implementation deficits in apraxia. Damage to the frontal and parietal lobes was more common in apraxics, but neither frontal nor parietal damage was associated with different arm movement deficits. Limb apraxia was associated with intact preprogramming but impaired response implementation. The response implementation deficits were characterized by spatial but not temporal deficits, consistent with decoupling of spatial and temporal features of movement in limb apraxia. While the apraxics’ accuracy was normal when visual feedback was available, it was impaired when visual feedback of either target location or hand position was unavailable. This finding suggests that ideomotor limb apraxia is associated with disruption of the neural representations for the extrapersonal (spatial location) and intrapersonal (hand position) features of movement. The non-apraxic group’s normal kinematic performance demonstrates that the deficits demonstrated in the apraxic group are not simply a reflection of left hemisphere damage per se.

Cortical networks underlying mechanisms of time perception

Authors:

• Deborah L. Harrington

• Kathleen Y. Haaland

• Robert T. Knight

Date: 1998

PubMed: 9437028

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Abstract:

Precise timing of sensory information from multiple sensory streams is essential for many aspects of human perception and action. Animal and human research implicates the basal ganglia and cerebellar systems in timekeeping operations, but investigations into the role of the cerebral cortex have been limited. Individuals with focal left (LHD) or right hemisphere (RHD) lesions and control subjects performed two time perception tasks (duration perception, wherein the standard tone pair interval was 300 or 600 msec) and a frequency perception task, which controlled for deficits in time-independent processes shared by both tasks. When frequency perception deficits were controlled, only patients with RHD showed time perception deficits. Time perception competency was correlated with an independent test of switching nonspatial attention in the RHD but not the LHD patients, despite attention deficits in both groups. Lesion overlays of patients with RHD and impaired timing showed that 100% of the patients with anterior damage had lesions in premotor and prefrontal cortex (Brodmann areas 6, 8, 9, and 46), and 100% with posterior damage had lesions in the inferior parietal cortex. All LHD patients with normal timing had damage in these same regions, whereas few, if any, RHD patients with normal timing had similar lesion distributions. These results implicate a right hemisphere prefrontal-inferior parietal network in timing. Time-dependent attention and working memory functions may contribute to temporal perception deficits observed after damage to this network.