A discussion of the neurological and pathophysiological basis of auditory hallucinations including musical hallucinations, tinnitus and psychotic hallucinations.

1. AUDITORY
HALLLUCINATIONS,
ILLUSIONS AND
DELUSIONS
Randy M Rosenberg MD FAAN FACP
Assistant Clinical Professor of Neurology
Lewis Katz School of Medicine atTemple University

2. Tinnitus
■ Auditory percept without an external source (mostly)
■ Aberrant activity originating in the auditory system
■ 10-15% prevalence in adults
■ 3% Interferes with Work, Sleep, Concentration, and Social
Interactions

3. TINNITUS

4. Tinnitus: Subjective and Objective

5. Hofmann, E; Behr, R; Neumann-Haefelin,T; Schwager, K
PulsatileTinnitus: Imaging and Differential Diagnosis
DtschArztebl Int 2013; 110(26): 451-8; DOI: 10.3238/arztebl.2013.0451

6. Causes of PulsatileTinnitus
■ Suggests involvement of blood flow through vessels near
the ear
– May be normal or pathological
■ Space-occupying lesions
■ Anemia
■ Overactive thyroid
■ Hypertension
■ Benign intracranial pressure

7. Muscle Protection of External Auditory Pathway

8. Otic Myoclonus

9. Palatal Myoclonus as a Cause ofTinnitus
■ Palatal myoclonus is a rare
cause of muscular-induced
clicking tinnitus.
■ It results from rhythmic
discharges from the inferior
olivary nucleus by a lesion in the
triangle of the Guillain-Mollaret
(brainstem).
■ The lesion is usually due
to stroke, trauma, multiple
sclerosis or degenerative
disease.
■ Some success has been
reported with botulinum toxin
injection therapy.

10. Red Flags inTinnitus
■ Sudden onset…with or without hearing loss
■ Unilateral tinnitus
■ Pulsatile tinnitus
■ Sudden tinnitus with stroke like symptoms

11. Pathophysiology of SubjectiveTinnitus
■ Although the pathological origin of tinnitus may be peripheral
(cochlear, 8th nerve), the perception is central
■ Neuroplasticity, the adaption of cortical and subcortical to
deprivation or distortion of sensory input from the damaged
cochlea==midbrain==auditory cortex
■ The auditory cortex that no longer receives stimulation due to
cochlear injury is called the lesion projection zone (LPZ)
■ Following cochlear injury, neurons in the LPZ change in two ways
– Increase in spontaneous firing rate
– Neurons that are adjacent to the LPZ represent a larger frequency
range
■ THE KEY UNDERSTANDING INTINNITUS RESEARCH ISTHAT
ALTHOUGHTINNITUS PRESENTS INTHE EAR, IT IS A
NEUROLOGICAL PHENOMENON

12. Role of the Basal Ganglion inTreatment

13. Diffuse Basal Ganglia Lesion
Case Report
• 63 M with chronic tinnitus, louder in
the poorer ear.
• Left sided CVA involving body of
caudate and adjacent subcortical
structures.
• Tinnitus suppressed completely.
• Asymmetric hearing loss remained
unchanged.
Lowry et al (2004) Otol Neurotol

14. Larson and Cheung (2012) Neurosurgery
Focal Basal Ganglia Lesion
Case Report
• 56 F with chronic tinnitus and
Parkinson’s disease.
• Left focal caudate infarction following
deep brain stimulation (DBS) lead
placement.
• Tinnitus suppressed substantially.
• Symmetric hearing loss remained
unchanged.

15. Basal Ganglia Medial Surface
1. Head of Caudate Nucleus
2. Body of Caudate Nucleus
3. Caudatolenticular Gray Bridge
4. Putamen
5. Tail of Caudate Nucleus
6. External segment of Globus
Pallidus
7. Internal segment of Globus
Pallidus
8. Amygdaloid Body
9. Nucleus Accumbens
Area
LC
CH
NA

16. Probe Delivers stimulation
to deep brain nuclei
Anchor Secures
Probe to the skull
Connector Establishes
link to the Controller
Programmer Communicates
with the Controller to customize
therapy
Controller Determines
parameters for brain
stimulation and houses the
power source
Deep Brain Stimulation System

17. MUSICAL HALLUCINATIONS
■ Affects 2% of patients with hearing loss
■ Purely nonpsychiatric
■ People highly dependent on their cell phones may
hallucinate their ringtones
■ The sounds are typically heard as short fragments of
simple melodies
– often from music heard regularly and familiar from youth
and especially from hymns and carols.
■ Hallucinations are pure and not contaminated or distorted
by the degree of current hearing loss
– This is similar to Charles Bonnet Syndrome

18. Musical Hallucinations
■ Charles Ives, Robert Schumann
■ Interfere with perception or conversation in a manner that never
occurs with normal musical imagery
■ Usually are a reference from the patient’s history of musical
exposure or training
– There are some patients who have musical hallucinations that they
cannot recognize but are familiar to those people around them
■ Characteristics changes over time
– Increasingly loud
– More intrusive
– Expanded repertoire with shorter duration
– Patient has limited options for control
Piano transcription of an musical hallucination

19. Musical Hallucinations
■ Can be a manifestation of partial seizures usually of right temporal origin
■ Drug induced
– Anticonvulsants
– Antidepressants
– Anesthetics
– Opiates
– Amandatine
■ Most common among hearing impaired suspected as a cortical release
phenomenon.
– Female > male
– Advanced age
■ NOT earworms

20. Earworms/Brainworms
■ Generally considered to be a
constant loop of fifteen to twenty
seconds of music lodged in your
head for at least a few hours, if not
days—or, in severe cases, months.
■ A particular hallmark of earworms
is the presence of passages with
closely spaced musical intervals
and long notes.
– In other words, a sequence in which
the notes are close to each other on
the music scale—such as C, C-sharp,
and D—and each note is held for a
moment before moving on to the
next.
■ Sing out loud!

21. ASMR: Autonomous Sensory
Meridian Response
■ A distinct, pleasurable tingling
sensation in the head, scalp, back, or
peripheral regions of the body in
response to visual, auditory, tactile,
olfactory, or cognitive stimuli
■ Whispering is the most frequently
cited stimulus
■ So SOUNDALONECAN INDUCE
PLEASUREWITHOUT BEING
MUSICAL! (FOR EXAMPLE…)

22. Symptoms of Schizophrenia
■ Positive
– Hallucinations (usually auditory)
– 70% of patient of which 40% are partially or fully refractory to drug therapy
– Delusions (fixed false beliefs)
– Disorganized speech and behavior
■ Negative
– Decreased emotional range
– Poverty of speech
– Loss of interests and drives
■ Cognitive deficits
■ Mood symptoms

23. Psychotic Auditory Hallucinations

24. Mesolimbic System

25. What Creates Positive Symptoms
Schizophrenia?
■ Abnormalities in the dopaminergic systems
– Drugs that diminish firing rates of mesolimbic dopamine D2 neurons are
antipsychotic
■ Hypodopaminergic activity in the mesocartical system lead to negative symptoms
■ Hyperdopaminergic activity in the mesolimbic systems leads to positive symptoms
■ Auditory/Verbal hallucinations may have an anatomical correlate with
hyperactivity in Wernicke’s area.
– rTMS (repetitive transcranial magnetic stimulation) at low frequencies (1Hzt)
targeting the superior temporal gyrus appear to improve symptoms

26. Transcranial Magnetic Stimulation and
Transcranial Direct Current Stimulation for
Auditory Hallucinations
■ tDCS appears as an emergent treatment for the management of auditory
hallucinations in schizophrenia, by means of the phenomenon of neuromodulation.
■ tTMS using MRI targeting of the left superior temporal lobe
■ 34% improvement in auditory hallucinations

27. Episodic Cranial Sensory Shock
(“Exploding Head Syndrome)
■ Benign condition in which a person hears loud "imagined" noises (such as a bomb
exploding, a gunshot, or a cymbal crash) or experiences an explosive feelingwhen
falling asleep or waking up.[
■ The most prevalent theory on the cause of EHS is dysfunction of the reticular
formation in the brainstem responsible for transition between waking and
sleeping.[2]
■ Paroxysmal sensory parasomnia not associated with significant pain.
■ Consider hypnagogic hallucinations and sleep paralysis as other parasomnias that
occur at the onset of sleep and before awakening
■ Treatment has included Anafanil, carbamazepine, methyphenidate. Reassurance
may be best approach.

28. Thanks for the time and the sounds…