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Letter to the Editor   |    
Astrocytic Activation as Evidence for Brain Damage
JOHN M. FRIEDBERG, M.D.
Am J Psychiatry 2005;162:195-b-196. doi:10.1176/appi.ajp.162.1.195-b

To the Editor: Andrew J. Dwork, M.D., et al. (1) found in their study that increased "cortical and hippocampal immunoreactivity for glial fibrillaryacidic protein…was most intense in thegroup that received ECT" (p. 576). They wrote that these "statistically significant" increases in glial fibrillary acidic protein "probably" indicated "widespread astrocytic activation." In other words, 5 weeks after the last ECT, they found abnormal tissue changes under the microscope that were made visible by specialized staining techniques. This makes sense. Astrocytic activation is the brain’s well-known pathological response to injury and disease of all kinds.

Astrocytic activation evidenced by increased glial fibrillary acidic protein has been found in multiple sclerosis (2), temporal lobe epilepsy (3), amyotrophic lateral sclerosis (4), systemic lupus erythematosus (5), human immunodeficiency virus dementia, Alzheimer’s dementia, and, of course, traumatic injury.

Astrocytic activation, then called reactive astrocytic gliosis, was found after ECT as far back as 1948 (6). This latest finding of astrocytic activation 5 weeks after ECT is additional robust evidence in favor of brain damage—not against it.

Dwork AJ, Arango V, Underwood M, Ilievski B, Rosoklija G, Sackeim HA, Lisanby SH: Absence of histological lesions in primate models of ECT and magnetic seizure therapy. Am J Psychiatry  2004; 161:576–578
[PubMed]
[CrossRef]
 
Malmeström C, Haghighi S, Rosengren L, Andersen O, Lycke J: Neurofilament light protein and glial fibrillary acidic protein as biological markers in MS. Neurology  2003; 61:1720–1725
[PubMed]
 
Briellmann RS, Kalnins RM, Berkovic SF, Jackson GD: Hippocampal pathology in refractory temporal lobe epilepsy: T2-weighted signal change reflects dentate gliosis. Neurology  2002; 58:265–271
[PubMed]
 
Lexianu M, Kozovska M, Appel SH: Immune reactivity in a mouse model of familial ALS correlates with disease progression. Neurology  2001; 57:1282–1289
[PubMed]
 
Trysberg E, Nylen K, Rosengren LE, Tarkowski A: Neuronal and astrocytic damage in systemic lupus erythematosus patients with central nervous system involvement. Arthritis Rheum  2003; 48:2881–2887
[PubMed]
[CrossRef]
 
Riese W: Report of two new cases of sudden death after electric shock treatment with histopathological findings in the central nervous system. J Neuropathol Exp Neurol  1948; 7:98–100
[PubMed]
 
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References

Dwork AJ, Arango V, Underwood M, Ilievski B, Rosoklija G, Sackeim HA, Lisanby SH: Absence of histological lesions in primate models of ECT and magnetic seizure therapy. Am J Psychiatry  2004; 161:576–578
[PubMed]
[CrossRef]
 
Malmeström C, Haghighi S, Rosengren L, Andersen O, Lycke J: Neurofilament light protein and glial fibrillary acidic protein as biological markers in MS. Neurology  2003; 61:1720–1725
[PubMed]
 
Briellmann RS, Kalnins RM, Berkovic SF, Jackson GD: Hippocampal pathology in refractory temporal lobe epilepsy: T2-weighted signal change reflects dentate gliosis. Neurology  2002; 58:265–271
[PubMed]
 
Lexianu M, Kozovska M, Appel SH: Immune reactivity in a mouse model of familial ALS correlates with disease progression. Neurology  2001; 57:1282–1289
[PubMed]
 
Trysberg E, Nylen K, Rosengren LE, Tarkowski A: Neuronal and astrocytic damage in systemic lupus erythematosus patients with central nervous system involvement. Arthritis Rheum  2003; 48:2881–2887
[PubMed]
[CrossRef]
 
Riese W: Report of two new cases of sudden death after electric shock treatment with histopathological findings in the central nervous system. J Neuropathol Exp Neurol  1948; 7:98–100
[PubMed]
 
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