1172
ANZJP Correspondence
Figure 1. Typical imaging findings of MLD. (A) Non-contrast CT brain demonstrates confluent bilateral periventricular deep white matter hypodensity (arrows) which is hypointense on T1 imaging without contrast enhancement (B) and hyperintense on T2 imaging (D). The abnormality spares the subcortical U fibres (arrowheads, inset B, D). Spectroscopy trace (C) demonstrates elevated myo inositol, reduced N-acetylaspartate and increased lactate.
disorder, were then attributed to a head injury, supported by an abnormal CT. The case highlights two important principles: first, the importance of a detailed history, which revealed that the behavioural and cognitive changes had occurred years after the head injury, and second, the utility of MRI compared with non-contrast CT. 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
aspartate), elevated myo-inositol and occasionally elevated lactate (Figure 1(c)) (Scott 2009).
Summary
Valproate for management of idiopathic olfactory hallucinosis
To the Editor
Shravani Chauhan1, Praveen Tripathi2, Amit Khanna2 and Priyanka Goyal2 1Department
of Psychiatry, VIMHANS, New Delhi, India 2Department of Psychiatry, IHBAS, New Delhi, India Corresponding author: Praveen Tripathi, Department of Psychiatry, IHBAS, DA-61, Shalimar Bagh, Delhi-110088, India. Email: [email protected] DOI: 10.1177/0004867414550210
John’s behavioural and affective changes, first diagnosed as a primary mood
Qualitative smell disorders like phantosmia are rarely reported in psychiatry (Nordin et al., 1996). Phantosmia is an olfactory hallucination without any olfactory trigger and must be differentiated from troposmia, which is distorted perception of an odorant stimulus. It may be the first sign of various neurological diseases (Majumdar et al., 2003); however, currently there is neither any good hypothesis regarding the pathophysiology of phantosmia nor any established treatment modality for long lasting phantosmia (Leopold, 2002).
Kumar V, Abbas A and Aster J. (2012) Robbins and Cotran Pathologic Basis of Disease, 9th ed. Philadelphia: Elsevier. Scott W (2009) Magnetic Resonance Imaging of The Brain and Spine 4th ed. Philadelphia: Lippincott, Williams and Wilkins. Van der Voorn JP, Pouwels PJ, Kamphorst W, et al. (2005) Histopathologic correlates of radial stripes on MR images in lysosomal storage disorders. AJNR American Journal of Neuroradiology 26: 442–446. Walterfang M, Mocellin R, Velakoulis D. (2009) Neuropsychiatric aspects of metabolic and endocrine disorder. In: Sadock BJ, Sadock VA, and Ruiz P (eds.) Kaplan and Sadock Textbook of Psychiatry. 9th edition. Sydney: Wolters Kluwer / Lippincott Williams and Wilkins, pp. 592–618.
A 42 year old female presented to the psychiatry outpatient department with complaints of perceiving a strong smell of onions episodically, each episode lasting around 10–15 minutes, for the last three years. The patient, in an attempt to get rid of this unpleasant smell, would wash her hands and household items, without any effect on the episodes. A diagnosis of OCD based on repeated washing behavior had been made earlier and the patient had received adequate trials of fluoxetine, sertraline and clomipramine without any improvement. There was no history of any other hallucinations or psychiatric complaints. These
Australian & New Zealand Journal ofDownloaded Psychiatry, 48(12) from anp.sagepub.com at HOWARD UNIV UNDERGRAD LIBRARY on March 10, 2015
1173
ANZJP Correspondence episodes were not associated with unresponsiveness or automatisms. There was no significant past or family history and she was not on any medications. The patient was provisionally diagnosed with idiopathic olfactory hallucinosis and, after ruling out depression and psychosis, her symptoms were thought to be either migrainous or epileptiform. Electroencephalography and magnetic resonance imaging were found to be normal. Results of hematological and serum biochemical analyses were normal. The patient was given a trial of valproate at a dosage of 800 mg/day. She showed significant improvement with marked decrease in both the number and duration of episodes. Valproate was continued and the patient showed sustained improvement in the hallucinations.
Cases of the above-mentioned olfactory hallucinosis are rarely seen in psychiatry clinics and the pathophysiology of olfactory hallucinations is far from clear. Some have suggested the activation of reverberating neuronal circuits such as in memory networks. The various possible mechanisms could be aberrant firing of action potentials at the periphery, loss of inhibitory fibers, abnormalities of the odor-binding proteins, disturbed central cortical processing or misinterpretation of other sensory signals (Majumdar et al., 2003). Several medications, including sedatives, anti-depressants and anti-epileptic drugs, have been suggested to treat olfactory distortions (Majumdar et al., 2003). In our case, absence of any imaging or electroencephalographic abnormalities and resolution of symptoms with anti-epileptic medications prompted us to consider that reverberating circuits and abnormal
signal generation may have been responsible for the hallucinations.
Late onset acute psychosis secondary to primary brain tumour: An initial misdiagnosis
week history of paranoid delusions, auditory hallucinations and pressure sores. He had a current diagnosis of bipolar I disorder, managed with olanzapine and sodium valproate since 2007. He recently had been non-compliant with his medications and recommenced cannabis use. Upon arrival to the emergency department, his symptoms were ascribed to a manic relapse of bipolar I disorder, with psychotic features, and he was admitted to the inpatient mental health unit. On psychiatric review four days later, AB described multiple paranoid delusions, including poisoning of his water supply, cameras in his light bulbs and that a gang of men had held him prisoner in his apartment, to which he attributed his pressure sores. He reported hearing God telling him of a highway accident, and elaborated with complex visual and auditory hallucinations involving him driving to the scene of the accident, personally comforting the victims and seeing the motor vehicles catch fire. His ex-wife reported that AB had been mentally stable, well and
ambulant four weeks previously. On physical examination AB had extensive necrotic pressure areas over his sacrum and thoracic spine and a widespread fungal infection over his buttocks. Biochemistry revealed raised urea and creatinine levels. The treating team diagnosed acute, late onset psychosis. A CT brain demonstrated a 4cm space occupying lesion in the right temporal lobe with significant surrounding oedema, marked midline shift and raised intracranial pressure. Medical review revealed right papilloedema, wide based gait and mild left sided hemiparesis. AB was urgently transferred to a neurosurgical unit, in which a biopsy revealed a stage four glioblastoma multiforme tumour. AB was not suitable for surgery, and subsequently returned to his hometown for palliative care. This case highlights the importance of not overlooking medical causes of first episode psychotic symptoms. Brain tumours are an uncommon, but important, cause of secondary psychosis (Keshavan and
Rebecca Kuehn Hunter New England Health District, NSW, Australia Corresponding author: Rebecca Kuehn, Calvary Mater Hospital, Waratah, Newcastle, NSW 2298, Australia. Email: [email protected] DOI: 10.1177/0004867414549964
To the Editor It is essential to determine if late onset psychosis is secondary to a medical condition, as patients may suffer undue morbidity and/or mortality if this is not identified. This is a case of late onset, acute psychosis in which an acute medical cause was not identified on initial presentation, leading to serious medical sequelae. AB is a 60 year old divorced male on welfare who presented to a rural hospital with a three to four
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 Leopold D (2002) Distortion of olfactory perception: Diagnosis and treatment. Chemical Senses 27: 611–615. Majumdar S, Jones NS, McKerrow WS, et al. (2003) The management of idiopathic olfactory hallucinations: A study of two patients. Laryngoscope 113: 879–881. Nordin S, Murphy C, Davidson TM, et al. (1996) Prevalence and assessment of qualitative olfactory dysfunction in different age groups. Laryngoscope 106: 739–744.
Australian & New Zealand Journal of Psychiatry, 48(12)
Downloaded from anp.sagepub.com at HOWARD UNIV UNDERGRAD LIBRARY on March 10, 2015
ANZJP Correspondence
Figure 1. Typical imaging findings of MLD. (A) Non-contrast CT brain demonstrates confluent bilateral periventricular deep white matter hypodensity (arrows) which is hypointense on T1 imaging without contrast enhancement (B) and hyperintense on T2 imaging (D). The abnormality spares the subcortical U fibres (arrowheads, inset B, D). Spectroscopy trace (C) demonstrates elevated myo inositol, reduced N-acetylaspartate and increased lactate.
disorder, were then attributed to a head injury, supported by an abnormal CT. The case highlights two important principles: first, the importance of a detailed history, which revealed that the behavioural and cognitive changes had occurred years after the head injury, and second, the utility of MRI compared with non-contrast CT. 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
aspartate), elevated myo-inositol and occasionally elevated lactate (Figure 1(c)) (Scott 2009).
Summary
Valproate for management of idiopathic olfactory hallucinosis
To the Editor
Shravani Chauhan1, Praveen Tripathi2, Amit Khanna2 and Priyanka Goyal2 1Department
of Psychiatry, VIMHANS, New Delhi, India 2Department of Psychiatry, IHBAS, New Delhi, India Corresponding author: Praveen Tripathi, Department of Psychiatry, IHBAS, DA-61, Shalimar Bagh, Delhi-110088, India. Email: [email protected] DOI: 10.1177/0004867414550210
John’s behavioural and affective changes, first diagnosed as a primary mood
Qualitative smell disorders like phantosmia are rarely reported in psychiatry (Nordin et al., 1996). Phantosmia is an olfactory hallucination without any olfactory trigger and must be differentiated from troposmia, which is distorted perception of an odorant stimulus. It may be the first sign of various neurological diseases (Majumdar et al., 2003); however, currently there is neither any good hypothesis regarding the pathophysiology of phantosmia nor any established treatment modality for long lasting phantosmia (Leopold, 2002).
Kumar V, Abbas A and Aster J. (2012) Robbins and Cotran Pathologic Basis of Disease, 9th ed. Philadelphia: Elsevier. Scott W (2009) Magnetic Resonance Imaging of The Brain and Spine 4th ed. Philadelphia: Lippincott, Williams and Wilkins. Van der Voorn JP, Pouwels PJ, Kamphorst W, et al. (2005) Histopathologic correlates of radial stripes on MR images in lysosomal storage disorders. AJNR American Journal of Neuroradiology 26: 442–446. Walterfang M, Mocellin R, Velakoulis D. (2009) Neuropsychiatric aspects of metabolic and endocrine disorder. In: Sadock BJ, Sadock VA, and Ruiz P (eds.) Kaplan and Sadock Textbook of Psychiatry. 9th edition. Sydney: Wolters Kluwer / Lippincott Williams and Wilkins, pp. 592–618.
A 42 year old female presented to the psychiatry outpatient department with complaints of perceiving a strong smell of onions episodically, each episode lasting around 10–15 minutes, for the last three years. The patient, in an attempt to get rid of this unpleasant smell, would wash her hands and household items, without any effect on the episodes. A diagnosis of OCD based on repeated washing behavior had been made earlier and the patient had received adequate trials of fluoxetine, sertraline and clomipramine without any improvement. There was no history of any other hallucinations or psychiatric complaints. These
Australian & New Zealand Journal ofDownloaded Psychiatry, 48(12) from anp.sagepub.com at HOWARD UNIV UNDERGRAD LIBRARY on March 10, 2015
1173
ANZJP Correspondence episodes were not associated with unresponsiveness or automatisms. There was no significant past or family history and she was not on any medications. The patient was provisionally diagnosed with idiopathic olfactory hallucinosis and, after ruling out depression and psychosis, her symptoms were thought to be either migrainous or epileptiform. Electroencephalography and magnetic resonance imaging were found to be normal. Results of hematological and serum biochemical analyses were normal. The patient was given a trial of valproate at a dosage of 800 mg/day. She showed significant improvement with marked decrease in both the number and duration of episodes. Valproate was continued and the patient showed sustained improvement in the hallucinations.
Cases of the above-mentioned olfactory hallucinosis are rarely seen in psychiatry clinics and the pathophysiology of olfactory hallucinations is far from clear. Some have suggested the activation of reverberating neuronal circuits such as in memory networks. The various possible mechanisms could be aberrant firing of action potentials at the periphery, loss of inhibitory fibers, abnormalities of the odor-binding proteins, disturbed central cortical processing or misinterpretation of other sensory signals (Majumdar et al., 2003). Several medications, including sedatives, anti-depressants and anti-epileptic drugs, have been suggested to treat olfactory distortions (Majumdar et al., 2003). In our case, absence of any imaging or electroencephalographic abnormalities and resolution of symptoms with anti-epileptic medications prompted us to consider that reverberating circuits and abnormal
signal generation may have been responsible for the hallucinations.
Late onset acute psychosis secondary to primary brain tumour: An initial misdiagnosis
week history of paranoid delusions, auditory hallucinations and pressure sores. He had a current diagnosis of bipolar I disorder, managed with olanzapine and sodium valproate since 2007. He recently had been non-compliant with his medications and recommenced cannabis use. Upon arrival to the emergency department, his symptoms were ascribed to a manic relapse of bipolar I disorder, with psychotic features, and he was admitted to the inpatient mental health unit. On psychiatric review four days later, AB described multiple paranoid delusions, including poisoning of his water supply, cameras in his light bulbs and that a gang of men had held him prisoner in his apartment, to which he attributed his pressure sores. He reported hearing God telling him of a highway accident, and elaborated with complex visual and auditory hallucinations involving him driving to the scene of the accident, personally comforting the victims and seeing the motor vehicles catch fire. His ex-wife reported that AB had been mentally stable, well and
ambulant four weeks previously. On physical examination AB had extensive necrotic pressure areas over his sacrum and thoracic spine and a widespread fungal infection over his buttocks. Biochemistry revealed raised urea and creatinine levels. The treating team diagnosed acute, late onset psychosis. A CT brain demonstrated a 4cm space occupying lesion in the right temporal lobe with significant surrounding oedema, marked midline shift and raised intracranial pressure. Medical review revealed right papilloedema, wide based gait and mild left sided hemiparesis. AB was urgently transferred to a neurosurgical unit, in which a biopsy revealed a stage four glioblastoma multiforme tumour. AB was not suitable for surgery, and subsequently returned to his hometown for palliative care. This case highlights the importance of not overlooking medical causes of first episode psychotic symptoms. Brain tumours are an uncommon, but important, cause of secondary psychosis (Keshavan and
Rebecca Kuehn Hunter New England Health District, NSW, Australia Corresponding author: Rebecca Kuehn, Calvary Mater Hospital, Waratah, Newcastle, NSW 2298, Australia. Email: [email protected] DOI: 10.1177/0004867414549964
To the Editor It is essential to determine if late onset psychosis is secondary to a medical condition, as patients may suffer undue morbidity and/or mortality if this is not identified. This is a case of late onset, acute psychosis in which an acute medical cause was not identified on initial presentation, leading to serious medical sequelae. AB is a 60 year old divorced male on welfare who presented to a rural hospital with a three to four
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 Leopold D (2002) Distortion of olfactory perception: Diagnosis and treatment. Chemical Senses 27: 611–615. Majumdar S, Jones NS, McKerrow WS, et al. (2003) The management of idiopathic olfactory hallucinations: A study of two patients. Laryngoscope 113: 879–881. Nordin S, Murphy C, Davidson TM, et al. (1996) Prevalence and assessment of qualitative olfactory dysfunction in different age groups. Laryngoscope 106: 739–744.
Australian & New Zealand Journal of Psychiatry, 48(12)
Downloaded from anp.sagepub.com at HOWARD UNIV UNDERGRAD LIBRARY on March 10, 2015
