959
ANZJP Correspondence At presentation no overt psychotic phenomenology was elicited. A diagnosis of antidepressant-induced hypomania was made. Agomelatine was ceased, and she was commenced on quetiapine 25mg nocte with gradual improvement in her symptoms over the following three weeks. Some months later however, she presented with an episode of overt mania in the absence of antidepressant therapy, supporting an underlying diagnosis of bipolar disorder. Risk factors for progression to manic switch include underlying Axis I mood disorder and younger age at the time of antidepressant introduction, with a higher risk of switch in bipolar disorder compared to major depressive disorder (Tondo et al., 2010). The timeframe for emergence of symptoms of hypomania or mania is variable. In the Systematic Treatment
Enhancement Program for Bipolar Disorder, a longitudinal cohort study, Perlis et al. (2010) found that amongst patients who transition from a depressive state directly to a manic, hypomanic, or mixed state, the median time to transition was 74 days. The role of antidepressants in bipolar depression remains a contentious issue and the subject of much debate. Tondo et al. (2010) noted that antidepressant-induced manic switch has been well reported with a number of antidepressant classes, including tricyclics, SSRIs, SNRIs, and MAOIs. The present case report suggests that agomelatine may also have the potential to precipitate manic switching. We suggest that, as with other antidepressants, all patients should be closely monitored during therapy for evidence of emerging hypomania or
mania, particularly in the setting of bipolar disorder and during the first few months of therapy initiation.
Neuropsychiatric symptoms as the presenting feature of acquired hepatocerebral degeneration Andrew Gleason2, Brad Hayhow1,2, Mark Walterfang1,2, Andrew Evans3, Ramon Mocellin1,2, Peter Gates4 and Dennis Velakoulis1,2
paranoia, grandiosity and aggression. He had no past psychiatric history and his family reported complete abstinence of alcohol in the preceding 2 months. On examination his sensorium was clear and there were no physical stigmata of hepatic dysfunction. He exhibited a slow, shuffling gait and slowed cognition, but smell was normal. On investigation his transaminases were only mildly elevated. Serum bilirubin and ammonia levels were normal, as were iron, copper and ceruloplasmin. Liver ultrasound was consistent with cirrhosis but showed no evidence of portal hypertension. No abnormalities were found on EEG or CT chest, abdomen and pelvis. MRI brain showed bilateral T1 hyperintensities in the caudate, putamen and globus pallidus (A). T2 signal in the same region was normal (B) (Figure 1). He was diagnosed with acquired hepatocerebral degeneration (AHD) secondary to alcoholic cirrhosis, and admitted to hospital for symptomatic treatment of his psychosis with haloperidol 2 mg daily. Three months later, the patient’s psychotic symptoms had resolved but he remained disinhibited and
demonstrated parkinsonism well in excess of expected medication sideeffects. Neuropsychological testing showed significantly impaired information processing speed, visuo-spatial functioning, working memory and executive functioning. Repeat MRI showed subtle improvement in basal ganglia hyperintensity (C). A more marked improvement at 9 months (D) was associated with improvements in both parkinsonism and cognition. AHD is a sub-acute variant of hepatic encephalopathy. It is not associated with delirium and can affect patients without overt clinical or biochemical evidence of hepatic failure (Ferrara and Jankovic, 2009). Cognitive symptoms include bradyphrenia and impairment of attention, with relative sparing of memory and language (Ferrara and Jankovic, 2009; Stracciari et al., 2008). Symmetrical parkinsonism is common on neurological examination, but chorea, dystonia, dyskinesia and ataxia may also occur (FernándezRodriguez et al., 2010; Ferrara and Jankovic, 2009). MRI shows distinctive T1 hyperintensity in the globus pallidi (Fernández-Rodriguez et al., 2010; Ferrara and Jankovic, 2009).
1Melbourne
Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Parkville, Australia 2Neuropsychiatry Unit, Royal Melbourne Hospital, Parkville, Australia 3Department of Neurology, Royal Melbourne Hospital, Parkville, Australia 4Department of Neuroscience, Barwon Health, Geelong, Australia Corresponding author: Andrew Gleason, Level 2, John Cade Building, Royal Melbourne Hospital, Melbourne, VIC 3050, Australia Email: [email protected] DOI: 10.1177/0004867414531079
To the Editor A 63-year-old man with a recent diagnosis of alcoholic cirrhosis presented to hospital with symptoms of acute
Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Perlis RH, Ostacher MJ, Goldberg JF, et al. (2010) Transition to mania during treatment of bipolar depression. Neuropsychopharmacology 35: 2545–2552. Tondo L, Vázquez G and Baldessarini RJ (2010) Mania associated with antidepressant treatment: comprehensive meta-analytic review. Acta Psychiatrica Scandanavica 121: 404-414.
Australian & New Zealand Journal of Psychiatry, 48(10)
Downloaded from anp.sagepub.com at University of New England on June 4, 2015
960
ANZJP Correspondence
Figure 1. MRI brain showing bilateral T1 hyperintensities in the caudate, putamen, and globus pallidus (A) with a normal T2 signal (B). Improvement in the T1 basal ganglia hyperintensity was seen at 3 months (C) and 9 months (D).
and intravenous use of manganesecontaminated drugs such as methcathinone (Fernández-Rodriguez et al., 2010; Ferrara and Jankovic, 2009). If left untreated the course is progressive, but symptoms, serum manganese levels and MRI changes all improve when hepatic function is restored (Ferrara and Jankovic, 2009). AHD is therefore an important differential diagnosis when seeking reversible causes of cognitive impairment in patients with alcoholic liver disease. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
The clinical and radiological features of AHD are associated with elevated manganese levels in the serum, CSF and globus pallidus on autopsy. Potential causes include impaired
biliary excretion and portosystemic shunting (Ferrara and Jankovic, 2009). A similar pattern is seen in manganese toxicity from occupational exposure, long-term total parenteral nutrition
Value of real world economic evaluations of crisis accommodation programmes for patients with severe mental illness Dan Siskind1,2,3, Meredith Harris1 and Harvey Whiteford1
To the Editor
1School
of Population Health, The University of Queensland, Brisbane St Lucia, Australia 2School of Medicine, The University of Queensland, Brisbane St Lucia, Australia 3Metro South Addiction and Mental Health Services, Woolloongabba, Australia Corresponding author: Dan Siskind, Queensland Centre for Mental Health Research, Level 3 Dawson House, The Park, Wacol, QLD 4076, Australia Email: [email protected] DOI: 10.1177/0004867414529478
We appreciate the comments provided by Dr Amos (Amos, 2014) regarding our evaluation of a crisis house for people with severe and persistent mental illness (Siskind et al., 2013). The core of Dr Amos’s comments relate to the difficulties in selecting appropriate controls from administrative data extracts for use in retrospective quasi-experimental evaluations of existing mental health services. While we agree that a limitation of this study was that there were differences between the intervention and control groups, we disagree with the view that no valid conclusions can be drawn from the study. In consultation with our statistical advisor, we believe that the statistical techniques used to
Fernández-Rodriguez R, Contreras A, de Villoria JG, et al. (2010) Acquired hepatocerebral degeneration: clinical characteristics and MRI findings. European Journal of Neurology 17: 1463–1470. Ferrara J and Jankovic J (2009) Acquired hepatocerebral degeneration. Journal of Neurology 256: 320–332. Stracciari A, Mattarozzi K, D’Alessandro R, et al. (2008) Cognitive functioning in chronic acquired hepatocerebral degeneration. Metabolic Brain Disease 23: 155–160.
adjust for differences between the intervention and control groups permit us to make meaningful economic interpretations of our results. There are inherent limitations when using retrospective administrative data. As variables cannot be prospectively selected, researchers must make interpretations form available data. Missing data can make certain variables unusable, as was the case for our data related to community clinical contacts. However retrospective administrative datasets allow for the evaluation of real world interventions. Insights into the efficacy of programmes targeted to actual public mental health service patients are inherently valuable as the results of randomised controlled trials with
Australian & New Zealand Journal of Psychiatry, 48(10) Downloaded from anp.sagepub.com at University of New England on June 4, 2015
ANZJP Correspondence At presentation no overt psychotic phenomenology was elicited. A diagnosis of antidepressant-induced hypomania was made. Agomelatine was ceased, and she was commenced on quetiapine 25mg nocte with gradual improvement in her symptoms over the following three weeks. Some months later however, she presented with an episode of overt mania in the absence of antidepressant therapy, supporting an underlying diagnosis of bipolar disorder. Risk factors for progression to manic switch include underlying Axis I mood disorder and younger age at the time of antidepressant introduction, with a higher risk of switch in bipolar disorder compared to major depressive disorder (Tondo et al., 2010). The timeframe for emergence of symptoms of hypomania or mania is variable. In the Systematic Treatment
Enhancement Program for Bipolar Disorder, a longitudinal cohort study, Perlis et al. (2010) found that amongst patients who transition from a depressive state directly to a manic, hypomanic, or mixed state, the median time to transition was 74 days. The role of antidepressants in bipolar depression remains a contentious issue and the subject of much debate. Tondo et al. (2010) noted that antidepressant-induced manic switch has been well reported with a number of antidepressant classes, including tricyclics, SSRIs, SNRIs, and MAOIs. The present case report suggests that agomelatine may also have the potential to precipitate manic switching. We suggest that, as with other antidepressants, all patients should be closely monitored during therapy for evidence of emerging hypomania or
mania, particularly in the setting of bipolar disorder and during the first few months of therapy initiation.
Neuropsychiatric symptoms as the presenting feature of acquired hepatocerebral degeneration Andrew Gleason2, Brad Hayhow1,2, Mark Walterfang1,2, Andrew Evans3, Ramon Mocellin1,2, Peter Gates4 and Dennis Velakoulis1,2
paranoia, grandiosity and aggression. He had no past psychiatric history and his family reported complete abstinence of alcohol in the preceding 2 months. On examination his sensorium was clear and there were no physical stigmata of hepatic dysfunction. He exhibited a slow, shuffling gait and slowed cognition, but smell was normal. On investigation his transaminases were only mildly elevated. Serum bilirubin and ammonia levels were normal, as were iron, copper and ceruloplasmin. Liver ultrasound was consistent with cirrhosis but showed no evidence of portal hypertension. No abnormalities were found on EEG or CT chest, abdomen and pelvis. MRI brain showed bilateral T1 hyperintensities in the caudate, putamen and globus pallidus (A). T2 signal in the same region was normal (B) (Figure 1). He was diagnosed with acquired hepatocerebral degeneration (AHD) secondary to alcoholic cirrhosis, and admitted to hospital for symptomatic treatment of his psychosis with haloperidol 2 mg daily. Three months later, the patient’s psychotic symptoms had resolved but he remained disinhibited and
demonstrated parkinsonism well in excess of expected medication sideeffects. Neuropsychological testing showed significantly impaired information processing speed, visuo-spatial functioning, working memory and executive functioning. Repeat MRI showed subtle improvement in basal ganglia hyperintensity (C). A more marked improvement at 9 months (D) was associated with improvements in both parkinsonism and cognition. AHD is a sub-acute variant of hepatic encephalopathy. It is not associated with delirium and can affect patients without overt clinical or biochemical evidence of hepatic failure (Ferrara and Jankovic, 2009). Cognitive symptoms include bradyphrenia and impairment of attention, with relative sparing of memory and language (Ferrara and Jankovic, 2009; Stracciari et al., 2008). Symmetrical parkinsonism is common on neurological examination, but chorea, dystonia, dyskinesia and ataxia may also occur (FernándezRodriguez et al., 2010; Ferrara and Jankovic, 2009). MRI shows distinctive T1 hyperintensity in the globus pallidi (Fernández-Rodriguez et al., 2010; Ferrara and Jankovic, 2009).
1Melbourne
Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Parkville, Australia 2Neuropsychiatry Unit, Royal Melbourne Hospital, Parkville, Australia 3Department of Neurology, Royal Melbourne Hospital, Parkville, Australia 4Department of Neuroscience, Barwon Health, Geelong, Australia Corresponding author: Andrew Gleason, Level 2, John Cade Building, Royal Melbourne Hospital, Melbourne, VIC 3050, Australia Email: [email protected] DOI: 10.1177/0004867414531079
To the Editor A 63-year-old man with a recent diagnosis of alcoholic cirrhosis presented to hospital with symptoms of acute
Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Perlis RH, Ostacher MJ, Goldberg JF, et al. (2010) Transition to mania during treatment of bipolar depression. Neuropsychopharmacology 35: 2545–2552. Tondo L, Vázquez G and Baldessarini RJ (2010) Mania associated with antidepressant treatment: comprehensive meta-analytic review. Acta Psychiatrica Scandanavica 121: 404-414.
Australian & New Zealand Journal of Psychiatry, 48(10)
Downloaded from anp.sagepub.com at University of New England on June 4, 2015
960
ANZJP Correspondence
Figure 1. MRI brain showing bilateral T1 hyperintensities in the caudate, putamen, and globus pallidus (A) with a normal T2 signal (B). Improvement in the T1 basal ganglia hyperintensity was seen at 3 months (C) and 9 months (D).
and intravenous use of manganesecontaminated drugs such as methcathinone (Fernández-Rodriguez et al., 2010; Ferrara and Jankovic, 2009). If left untreated the course is progressive, but symptoms, serum manganese levels and MRI changes all improve when hepatic function is restored (Ferrara and Jankovic, 2009). AHD is therefore an important differential diagnosis when seeking reversible causes of cognitive impairment in patients with alcoholic liver disease. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
The clinical and radiological features of AHD are associated with elevated manganese levels in the serum, CSF and globus pallidus on autopsy. Potential causes include impaired
biliary excretion and portosystemic shunting (Ferrara and Jankovic, 2009). A similar pattern is seen in manganese toxicity from occupational exposure, long-term total parenteral nutrition
Value of real world economic evaluations of crisis accommodation programmes for patients with severe mental illness Dan Siskind1,2,3, Meredith Harris1 and Harvey Whiteford1
To the Editor
1School
of Population Health, The University of Queensland, Brisbane St Lucia, Australia 2School of Medicine, The University of Queensland, Brisbane St Lucia, Australia 3Metro South Addiction and Mental Health Services, Woolloongabba, Australia Corresponding author: Dan Siskind, Queensland Centre for Mental Health Research, Level 3 Dawson House, The Park, Wacol, QLD 4076, Australia Email: [email protected] DOI: 10.1177/0004867414529478
We appreciate the comments provided by Dr Amos (Amos, 2014) regarding our evaluation of a crisis house for people with severe and persistent mental illness (Siskind et al., 2013). The core of Dr Amos’s comments relate to the difficulties in selecting appropriate controls from administrative data extracts for use in retrospective quasi-experimental evaluations of existing mental health services. While we agree that a limitation of this study was that there were differences between the intervention and control groups, we disagree with the view that no valid conclusions can be drawn from the study. In consultation with our statistical advisor, we believe that the statistical techniques used to
Fernández-Rodriguez R, Contreras A, de Villoria JG, et al. (2010) Acquired hepatocerebral degeneration: clinical characteristics and MRI findings. European Journal of Neurology 17: 1463–1470. Ferrara J and Jankovic J (2009) Acquired hepatocerebral degeneration. Journal of Neurology 256: 320–332. Stracciari A, Mattarozzi K, D’Alessandro R, et al. (2008) Cognitive functioning in chronic acquired hepatocerebral degeneration. Metabolic Brain Disease 23: 155–160.
adjust for differences between the intervention and control groups permit us to make meaningful economic interpretations of our results. There are inherent limitations when using retrospective administrative data. As variables cannot be prospectively selected, researchers must make interpretations form available data. Missing data can make certain variables unusable, as was the case for our data related to community clinical contacts. However retrospective administrative datasets allow for the evaluation of real world interventions. Insights into the efficacy of programmes targeted to actual public mental health service patients are inherently valuable as the results of randomised controlled trials with
Australian & New Zealand Journal of Psychiatry, 48(10) Downloaded from anp.sagepub.com at University of New England on June 4, 2015
