Approaching catatonia from a circuits perspective, C. Miller Fisher4 proposed that catatonic depression emerged from connection disturbances in the same mesoencephalofrontal system (brainstem to basal ganglia to limbic system and cerebral cortex) that also leads to akinetic mutism. Northoff5 used neuroimaging in patients recovering from catatonia to uncover trait features through provocative testing of response to fearful faces and situations. He described a region of interest in the orbitofrontal cortex that overreacts in these provocative situations, which suggests dysfunctional responsiveness.
Other functional imaging studies have shown altered activity in orbitofrontal, prefrontal, parietal, and motor cortical regions.6 Recently, T1-weighted MRI imaging in catatonia secondary to schizophrenia spectrum disorders showed reduced cortical thickness in frontoparietal regions as well as hypergyrification in the anterior cingulate cortex and medial orbitofrontal cortex compared with controls.7 The basal-ganglia-thalamo-cortical loop system has been implicated in the pathophysiology of catatonia, with interruption at various nodes leading to specific symptoms of catatonia.8 For example, disruption to the anterior cingulate cortex circuit may contribute to akinesia and mutism; to the lateral orbitofrontal circuit, echophenomena; and to the supplementary motor area circuit, increased tone. Integration of these hypotheses comes closest to offering a putative pathophysiological understanding of the mystery of catatonia.
Catatonia as a syndrome may arise from multiple etiologies and can lead to medical complications that result in significant morbidity and mortality, making rapid diagnosis and treatment a priority. Medical complications abound, and the mortality rate for malignant catatonia despite better recognition and treatment is still 9% to 10%.9 For a list of potential medical complications, see Table 2.
Catatonia has several mimics, which must be ruled out before making a diagnosis. Locked-in syndrome, linked to pontine lesions, can be distinguished from catatonia because patients will generally attempt to communicate with their eyes. Patients in a persistent vegetative state may also appear to be catatonic. Stiff person syndrome is an autoimmune disorder that presents during severe stress with intense lower extremity spasmodic stiffness that may appear like catatonic posturing, but these patients speak and complain about their pain.
Some patients suspected of being in a catatonic state may have an extrapyramidal parkinsonism. These can have a distinctive tremor but are not negativistic and lack bizarre catatonic psychomotor symptoms. Nonconvulsive status epilepticus can also produce a catatonic-like state; electroencephalography is essential for accurate diagnosis and prompt management may minimize cognitive damage.
Dr Beach is Assistant Professor of Psychiatry and Residency Training Director, Massachusetts General Hospital, Harvard Medical School; Dr Francis is Professor of Psychiatry, Associate Director of Residency Training, and Director of Neuromodulation Services, Penn State Medical School, Hershey Medical Center, Hershey, PA; Dr Fricchione is Professor of Psychiatry, Mind Body Medical Institute and Associate Chief of Psychiatry, Massachusettes General Hospital, Harvard Medical School, Boston, MA. Drs Fricchione and Beach have received funding through the David Judah Fund for catatonia research.
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