Postgraduate seminar Date: 2 August 2018 Venue: Meeting Room, Dept of Psychiatry, School of Medical Sciences, USM

1. VISUAL HALLUCINATIONS :
DIFFERENTIAL DIAGNOSIS &
TREATMENT
Presented by : Dr. Rahmat Hidayat Roslan
Supervisor : Prof Madya Dr. Zahiruddin Othman
2nd August 2018

3. OUTLINE
 Introduction
 Types of Visual Hallucinations
 Etiology of Visual Hallucinations
 Differential Diagnosis for Visual Hallucinations
 Treatment for Visual Hallucinations
 References

4. INTRODUCTION

5.  Visual Hallucination : A History
- 2 clinical reviews were published in 1936 about
approaching VH :
1. Swiss Medical Journal by George de Morsier
2. French Journal by Jean L’Hermitte and Juliann de
Ajuriaguerra
- VH were deemed worthy of study in their own right.
Distinct from other types of hallucinations.
- They were to be considered as unitary symptom.
- Distance VH from VI  higher clinical status
*However, both papers differ in conceptions of the brain
and its disorders.

6.  De Morsier described a set of VH syndromes based on
wider neurological and psychiatric context  relevant
until today
 One sparked 70 years of controversy
 What is it??
CHARLES BONNET
SYNDROME

7. WHAT IS VISUAL HALLUCINATION?
 A perception of an external visual stimulus where
none exists.
 Clinical manifestation of neuroophthalmologic
dysfunction resulting from a wide variety of
underlying etiologies.
 Not a pathognomonic of primary psychiatric illness.

9. CATEGORIES OF VISUAL HALLUCINATION
VH
Simple
Phosphenes Photopsias
Complex
Formed

10. WHAT CAUSES VISUAL HALLUCINATIONS?
 Numerous hypotheses have been suggested.
1. Psychophysiologic – disturbance of the brain
structure
2. Psychobiochemical – disturbance of
neurotransmitters
3. Psychodynamic – emergence of the unconscious
into consciousness.
 VH can be the result of all 3 processes.

11.  Until now, there is no single neural mechanism explaining
the types of VH.
 However, the similarity of VH that are associated with
seemingly diverse condition suggests a final common
pathway.
 Manford and Andermann (1998) summarized 3
mechanism for complex VH.

12.  Mechanism 1
- Irritation of cortical centres responsible for visual
processing.
- Irritation of primary visual cortex (Broadmann’s area 17)
 simple elementary VH.
- Irritation of visual association cortices (Broadmann’s area
18 and 19) causes more complex VH.
- Can be supported by EEG and direct stimulation
experiments.

13.  Mechanism 2
- Lesions that cause deafferentation of the visual system
may lead to cortical release phenomenon including VH.
- Deafferented neurons undergo specific biochemical and
molecular changes  increase in excitability (similar to
the denervation hypersensitivity seen in phantom limb
syndrome.
- Multitude of lesions can cause loss of input and inhibit
other cognitive functions
- Eg: it can be induced by prolonged visual deprivation.

14.  Mechanism 3
- Reticular activating system has its role in maintenance of
arousal  genesis of VH.
- As such, lesions of the brainstem have led to VH as in
peduncular hallucinosis.

15. IN WHAT CONDITIONS VH CAN BE
PRESENTED?
ORGANIC ??
FUNCTIONAL ??

16. RETINA PATHOLOGY
 Traction, irritation, injury or any disease of the retina
can stimulate retinal photoreceptors  simple
hallucinations.
 Posterior vitreous detachment (PVD) producing
traction of the retina is a common cause of retinal
hallucinations especially in older patients.
 VH are never complex.
 Insight is usually intact.
 Valsalva-like maneuvers can trigger VH in retinal
traction.

17.  Duration of hallucination is usually measured in seconds.
 Variable frequency.
 More frequent and persistent VH are associated with
Acute Zonal Occult Outer Retinopathy (AZOOR) or
cancer-associated retinopathies.
 If scotoma develops after the onset of VH, this means a
retinal injury occurred and may become permanent if not
evaluated and treated promptly.
 Note : all hallucinations suspected to retinal origin, urgent
ophthalmologic evaluation should be prompted to ensure
the retina is intact.
 Formal visual field test, electroretinogram, serum studies
for antibodies against retinal protein are suggested in
revealing the retinal dysfunction.

20. CHARLES BONNET SYNDROME
 Aka release hallucinations.
 Visual acuity loss or visual field loss from any
cause.
 Affecting the eye, optic nerve, optic chiasm, tract,
optic radiations or the visual cortex  VH
 Most reported in elderly patients.
 Age related macular degeneration, glaucoma,
diabetic retinopathy, and cerebral infarction.
 Risk factor : cognitive impairment and social
deprivation.
 VH can be simple or complex.
 Insight is usually retained.

22. MIGRAINE
 Prevalence of migraines in the general population has been
reported as between 15-29%.
 Up to 31% of those with migraine have an aura.
 Nearly all (99%) reported to have visual symptoms associated
with aura.
 Pathophysiology of aura is still not well understoood.
 The classic aura starts as a flickering, uncoloured, unilateral
zig-zag line in the centre of the visual field >> gradually
progress to the periphery  leaving scotoma.
 Duration : approximately 30 minutes.
 Can also include vision loss and visual distortions
(appearance of heat waves).
 fMRI can show the spreading cortical depression.
 It involves with the brief period of hyperperfusion followed by
slow spreading wave of hypoperfusion.

23. Source localization and time of onset of the MR signal perturbations.
Nouchine Hadjikhani et al. PNAS 2001;98:8:4687-4692
©2001 by National Academy of Sciences

24.  Common associated symptoms include headache,
nausea, vomiting, photophobia, phonophobia.
 No diagnostic test for migraine.
 ICHD-3 require 2 attacks of aura with fully reversible
symptoms of either visual, sensory, motor, brainstem
or speech disturbance, with at least 2 of the following
features:
- At least one aura symptoms spread gradually over > 5
mins
- Each individual aura symptom lasts for 5-60 mins.
- At least one aura symptom is unilateral.
- The aura is accompanied or followed within 60 mins by
headache.

25.  How to treat migraine aura?
- Verapamil may be useful as a prophylactic treatment.
- Others reported, agent with efficacy for persistent visual
aura include acetazolamide, lamotrigine, valproate.

26. SEIZURE
 VH of epileptic origin have often been described as simple, brief, and
consistent; could be complex as well.
 Consist of small, brightly coloured spots or shapes that flash.
 Usually localized to the occipital, occipitotemporal and
occipitoparietal regions of the cortex.
 Content of VH may be distorted in size, or suddenly change shape,
moving from lateral to the centre of the field of vision.
 Associated symptoms such as déjà vu, somatosensory phenomena,
head and eye deviation, motor activity and/or impaired
consciousness.
 Postictal headache is common in occipital epilepsy – hard to
differentiate between migraine headache.
 Complete neurological evaluation and EEG should be performed.
 Treatment?? Antiepileptic medications
- Valproate
- Phenytoin
- Etc
Neuroleptic if inter ictal

27. DEMENTIA WITH LEWY BODIES/PD
 The 2nd most common form of dementia.
 VHs are a core clinical feature of DLB (>20%) and also
common in PD.
 VH involve seeing objects move when they are actually still
and seeing complex scenarios of people and items that are
not present.
 Insight may or may not retained.
 In DLB, the VH occur early in the disease course while in PD
they come later.
 Risk factors for VH in PD include the high doses of
antiparkinson drugs, dementia itself, advanced age, impaired
vision, depression, and sleep problem.
 Treatment ?? 1. Cholinesterase inhibitor such as
Rivastigmine, donepezil
2. Neuroleptic such as Seroquel or
Clozapine

28. OTHER TYPE OF DEMENTIA?
 VHs are relatively uncommon in AD.
 If present, these often reflect a superimposed
delirium, medication effect, or vision loss.
 VHs are also rare in FTD.
 Some patients with Creutzfeldt-Jakob Disease
(CJD) present with prominent visual symptoms that
VH. Typically it will progress rapidly to dementia
and myoclonus.

29. DELIRIUM
 A syndrome that involves an acute disturbance of
consciousness; diminished ability to sustain
attention
 Caused by medical conditions, metabolic
disturbances, infections, drug effects, intracranial
processes.
 VH is the common type of hallucination that occur
in delirium, occurring around 27% in hospitalized
patients.
 Patients typically are confused, often agitated with
other psychotic symptoms such as TH, AH and
delusions.

30. ALCOHOL AND DRUG USE OR WITHDRAWAL
 VH can be simple or complex.
 Alcohol and benzodiazepine withdrawal usually
produce complex hallucinations with vivid imagery.
 It is continuous and associated with agitation,
tremulousness and autonomic hyperactivity.

31. Copyrights apply

32.  Most VH caused by medications or recreational drug use
are associated with acute intoxication.
 Also associated with confusion (delirium) often with AH
and TH.
 Digoxin and sildenafil can affect retinal function and
produce simple hallucination.
 For most medication-induced hallucinations, dose-
lowering or discontinuation of the drug may be
necessary.

33. PEDUNCULAR HALLUCINOSIS
 A rare manifestation of lesions (usually stroke or
neoplasm) affecting the midbrain  paramedian
reticular formation.
 VH arise following the infarct of the midbrain.
 VH can be complex, content of the imagery varies and is
usually described as colourful and vivid.
 It usually start within a few days of the initial insult and
resolve within a few weeks >> may last for years.
 It may be associated with TH and AH.
 Other associated symptoms such as sleep disturbance,
eye movement disturbance, ataxia, hemiparesis and
confusion.
 Insight is variably retained.
 Neuroimaging is essential for detection.

35. NARCOLEPSY
 VH of are usually complex, vivid, coloured images,
invariably occurring immediately before falling asleep
(hypnagogic -37%), or just after wakening (hypnopompic
– 12.5%).
 Associated symptoms include excessive daytime
sleepiness, sleep paralysis, and cataplexy.
 Poor insight may occur because of the very realistic
imagery from the VH, however most patients know the
hallucinations are not real.
 Medication that disrupt sleep architecture (eg:
serotonergic and anticholinergic antidepressants) can
also produce hypnagogic and hypnopompic
hallucinations.
 Diagnostic testing includes an overnight polysomnogram
followed by multiple sleep latency test.

37.  Treatment ??
- Non-pharmacological approach
- Pharmacological approach
1. Avoidance of certain drugs
2. Sleep hygiene
3. Psychosocial support
1. Modafinil – non amphetamine
2. Methylphenidate
3. Antidepressant if associated
with cataplexy

38. PSYCHIATRIC ILLNESS
 Most VH are complex.
 Involving vivid scenes with family members, religious
figures and animals.
 Reaction to these VH can vary include fear, pleasure or
indifference.
 Reported in 16-72% of patients with schizophrenia and
schizoaffective disorder.
 Many but not all, patient with psychiatric illness lack
insight.
 Complete psychiatric evaluation is essential
 Treatment ??
Neuroleptics

39. Copyrights apply

40. EVALUATION
 VHs are under reported by patients who fear that
the hallucinations represent psychiatric illness.
 Insight is an important feature that can distinguish
among some etiologies.
 Patient should be asked to describe their
hallucinations.

41.  Specific enquiry :
- Monocular vs binocular involvement
- Involved area of the visual field
- Motion
- Triggers
- Duration
- Frequency
- Associated symptoms and medical hx
- insight

42. DIAGNOSTIC TESTING
 All patients with new onset of VH should have a
 Don’t forget the screening for cognitive impairment,
parkinsonism, other neurologic deficits.
 Medication lists should be reviewed thoroughly.
 Serum for drugs or urine toxicology for detection.
Complete neurologic
evaluation

43.  New onset of simple VH that are monocular should have
an urgent ophthalmologic examination.
 Simple VH that meet the criteria for migraine may not
require further diagnostic evaluation.
 EEG is indicated when the episodes are brief, frequent
and stereotyped >> seizure.
 MRI is appropriate when hallucinations do not meet the
criteria for visual aura of migraine + when the neurologic
examination is abnormal.

44. Copyrights apply

45. HOW ARE VISUAL HALLUCINATIONS TREATED

46. REFERENCES
 Pelak VS, Brazis PW, Wilterdink JL. Approach to the patient with
visual hallucinations . Uptodate 2016:
https://ezproxy.usm.my:4243/contents/approach-to-the-patient-with-
visual-
hallucinations?search=visual%20hallucinations&source=search_resu
lt&selectedTitle=1~130&usage_type=default&display_rank=1
 Teeple RC, Caplan JP, Stern TA. Visual Hallucinations : Differential
Diagnosis and Treatment. The Primary Care Companion to the
Journal of Clinical Psychiatry 2009:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2660156/
 Ffytche DH. Visual Hallucinatory Syndromes: past, present and
future. Clinical Research 2007; 173-178

47. THANK YOU