Catatonia Eight Years after Head Injury

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*Corresponding author: E-mail: rbota@uci.edu;
British Journal of Medicine & Medical Research
19(4): 1-12, 2017; Article no.BJMMR.30545
ISSN: 2231-0614, NLM ID: 101570965
SCIENCEDOMAIN international
www.sciencedomain.org
Catatonia Eight Years after Head Injury
Leonard Groysman
1
, Keeban Nam
2
, Nancy Vo
3
, Evita Rocha
2
, Jessica Cvetko
2
,
Jessica Kim
2
, Ebaa Al-obeidi
3
, Christopher Cho
2
and Robert G. Bota
2*
1
Department of Neurology, University of California, Irvine, USA.
2
Department of Psychiatry, University of California, Irvine, USA.
3
Medical School, University of California, Irvine, USA.
Authors’ contributions
This work was carried out in collaboration between all authors. Author LG redesigned and rewrote parts of
the paper and formulated the strategies of interventions. Authors KN, NV, ER, JC, JK, EAO and CC wrote
parts of the manuscript, did the literature search, prepared the tables and contributed significantly through
the process. Author RGB designed the study, coordinated the process and wrote parts of the manuscript.
All authors read and approved the final manuscript.
Article Information
DOI: 10.9734/BJMMR/2017/30545
Editor(s):
(1) Thomas I. Nathaniel, University of South Carolina, School of Medicine-Greenville, Greenville, SC 29605, USA.
Reviewers:
(1) Valentina Galetto, University of Turin, Italy.
(2)
John E. Berg, Oslo and Akershus University, Norway.
Complete Peer review History:
http://www.sciencedomain.org/review-history/17300
Received 16
th
November 2016
Accepted 10
th
December 2016
Published 21
st
December 2016
ABSTRACT
We present the case of a male patient with traumatic brain injury leading to gradual deterioration in
functioning over several years, culminating in a state of prolonged treatment-resistant catatonia
complicated by an inability to perform activities of daily living and necessitating total care by
nursing staff. Extensive diagnostic evaluation did not reveal a convincing etiology of patient’s
catatonia. Despite several empiric treatment modalities administered early in the course of
catatonia, patient’s condition continued to decline. We did not observe sustained changes in
response to high dose lorazepam, selegiline/minocycline coadministration, or ECT alone, but
rather exponential improvement from the combination of medications and ECT.
Keywords: Catatonia; traumatic brain injury; ECT; monoamine oxidaze.
Case Study

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1. INTRODUCTION
Traumatic brain injury (TBI) is a common
condition and a significant cause of morbidity and
mortality. The Centers for Disease Control and
Prevention (CDC) has recognized the need to
reduce the burden of unintentional injuries and
their long term consequences [1]. The CDC
initiatives focus on multiple aspects ranging from
identification and prevention of TBI, recognition
and management and interventions to improve
long term health outcomes [1].
Catatonia is a less studied consequence of TBI
[2]. The paucity of reports of TBI related
catatonia could be due to a multitude of medical
problems from initial trauma and significant
anatomical variability of injuries and diversity of
clinical presentations masking the syndrome.
However, TBI patients exhibited EEG patterns
suggestive of diminished inter-hemispheric
coordination. These abnormal findings were
associated with weakened structural integrity of
white matter tracts [3]. In Franke et al., blast-
related mild traumatic brain injury (mTBI) was
associated with increases in low frequency
power on EEG [4]. Through an EEG index, it was
found that EEG was able to distinguish between
severities of mTBI and was sensitive to detect
injury effects six months after their mTBI, notable
for an increase in slower frequency activity
revealing information to abnormalities in the
blood brain barrier [5]. In Sponheim et al., two
and a half years after injury there was reported
decreased frontal phase synchrony on EEG [6].
Slow oscillations have been positively correlated
with increased frontal white matter T2 relaxation
time in moderate to severe TBI, possibly
suggesting reduced white matter excitatory
cortical input [4]. In severe TBI patients
who completed rehabilitation and made
cognitive gains as in Castellanos et al., there
was a decrease in low-frequency connectivity
[7]. Overall as in Franke et al., EEG changes
are appreciable in the chronic period and
can be useful for tracking the course of
recovery and enduring susceptibilities to injury
[4].
The dynamic characteristics of the EEG allow
one to characterize the severity of the patient’s
current state, the ability to identify brain
structures, and to define cortical lesions [8]. As in
Sharova et al., the most important prognostic
factors were found to be the baseline and
reactive frequency characteristics of the EEG
power spectrum, particularly when assessed two
to three months after a trauma [8].
2. CASE REPORT
Mr A is a 26-year-old Caucasian male who
presented to the emergency room at the
University of California, Irvine (UCI) with
symptoms of mutism, rigidity, withdrawal,
negativism, and waxy flexibility.
Eight years prior to the admission he had a
traumatic brain injury from a motor vehicle
accident. After recovery from his injuries, he was
able to complete high school and a four-year
college. During this time, his family noticed a
progressive deterioration in functioning, bursts of
irritability and anger. After graduation from
college, the patient was not able to find
employment for 2-3 years. He became
increasingly withdrawn; at times he would not
talk for days. The duration and frequency of
episodes of mutism increased in the following
months, worsening to the point that he would not
speak at all and required prompting for all
activities. At this juncture, he was admitted for
investigations at a large private hospital (see
Table 1 for list of workup completed). Shortly
after, he was again hospitalized for an extensive
three-week workup at another private hospital
(see Table 2 for the list of workup done). The
following tests were notable: low IgA, positive
streptococcus antibody screen with elevated
ASO titers, positive CSF anti-neuronal
antibodies, and mildly elevated alpha-1 and -2 on
serum protein electrophoresis. Magnetic
resonance imaging (MRI) showed mild cerebellar
atrophy not different than the MRI one year
before and continuous EEG showed the
presence of very mild slowing. He was subjected
to the following treatments: amoxicillin-
clavulanate, tinidazole, a course of intravenous
immunoglobulin (IVIG), lorazepam 1 mg every
four hours via intravenously, olanzapine,
mirtazapine, and methylprednisolone, with no
clinical effect.
At the time of admission to UCI, there were
several failed the attempts to find a definitive
diagnosis. The patient showed progressive
deterioration despite treatment. As he had no
oral intake for days prior to the admission, the
patient was started on lorazepam, titrated to 10
mg a day, and showed improvement in oral
intake. However, the patient would not take per
os medications requiring him to receive the

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Lorazepam intramuscularly. Subsequently, the
patient was transferred to the intensive care unit
for continuous monitoring. Lorazepam was
increased to at a total dose of 72 mg a day with
debatable further improvement in symptoms.
Trials of Olanzapine or lithium did not show
significant benefit.
After transfer back to medical psychiatry unit
selegiline was started and titrated up to 12 mg a
day, along with a lorazepam dose of 4 mg a day.
ECT was started and by the second treatment,
the Bush-Francis score decreased from 34 to 24.
However, medications had to be stopped as his
legal status changed requiring the team to apply
for another permission from the court to give
medications. During those four days, the patient
continued to receive ECT; however his Bush-
Francis catatonia score returned to the previous
level. After we restarted his medications, we also
added minocycline 100 mg PO twice a day, and
continued the ECT as scheduled, at three times
a week. His catatonia score decreased to 23, 14
and then 0, with these scores determined within
a two-day interval. Four days later he began
speaking in full sentences, became cooperative
with staff and no longer required a sitter. For the
following week, he maintained his significant
clinical improvement with continued gradual
improvement. He received a total of nine bilateral
ECT treatments. Due to his significant
improvement, the patient and the family declined
further ECT treatment.
He was discharged with follow-up at a partial
hospitalization program (PHP). From this point
on, the Montreal Cognitive Assessment remained
at 30. Patient continued to do well for one month,
at which time he started to again display
catatonic symptoms. At a follow-up appointment,
it was discovered that the patient had decreased
medication compliance in the week prior.
Fortunately, the symptoms resolved in two days,
but just weeks later reemerged- only to identify
that the cause was likely decrease in the
frequency of PHP program from five days to
three days. The increase in days led to the
symptom resolution. A few weeks later the
frequency was decreased to three days a week
uneventfully.
3. DISCUSSION
The brain is an electro-chemical organ. The
implication of this is multifaceted. Understanding
the TBI related brain changes is paramount. The
clinical course over the eight years starting with
severe TBI and progressing to treatment-
resistant catatonia is just an example of often
subtle but pervasive long term effects of brain
injury. We believe that catatonia secondary to
TBI should be considered in similar patient
population if no other plausible causes are
identified.
There are anecdotal reports of catatonia
following TBI [9-11], including one case in which
a 15 year-old patient made a full recovery only to
develop catatonia and psychosis ten months
later [12]. Another published case described a
patient who sustained a head injury followed by a
gradual decline in academic performance [13].
Two years after the injury, the patient developed
an abrupt onset of irrational speech, irritability,
and negativism. Over the next few years he
developed signs of catatonia; resistant to
benzodiazepines but successfully treated with
risperidone. Another publication described a
patient with a TBI who developed atypical
catatonia consisting of primarily language
processing and social interaction deficits that
responded well to lorazepam [14]. A related
syndrome known as lethal catatonia, in which
fever and hyperactivity progress to stuporous
exhaustion, has also been found to follow TBI
[11]. In a retrospective study assessing the
etiologies of catatonia in 75 consecutive cases,
Smith, et al., identified six patients who had a
history of traumatic brain injury [10]. Similarly,
Wilcox, J.A. found catatonic patients were more
likely to have had a prior history of brain injury
when compared to manic, depressed or surgical
patients used as controls [15]. Ahuja N. proposed
that a common theme in the origin of organic
catatonia was lesions in and around the third
ventricle [16].
There is no consensus on how to treat catatonia
in persons with brain injuries; however, clozapine
and risperidone have been found to be effective
in some cases where benzodiazepines failed [9
17]. For example, Rommel and colleagues
described a woman involved in a major motor
vehicle accident that caused frontal lobe injury
and subsequently catatonia one month later who
was effectively treated with clozapine [9].
Minimally-responsive head injury survivors may
have chronic catatonia reversed years after an
accident [18].
At the climax of his catatonia, Mr. A did not
respond to single treatment modalities, e.g.,
medication, ECT or behavioral interventions, but
a combination of all.

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Table 1. Diagnostic testing at the first private hospital
Total hospital days: 3
Date
Diag
nostic tests
Results
Normal range
HD*1 IgA – low <40 70-400 mg/dL
IgG 971 700-1600 mg/dL
IgM 152 40-230 mg/dL
TSH .65 .46-4.68 uIU/mL
HD1
Streptococcal Ab* screen
Positive
Negative
ASO semi-qnt titer – elevated 400 <200 IU
HD2 Lumbar puncture, CSF Glucose: 54
Protein: 47
RBC 30, WBC 1
Clear & colorless
40-70 mg/dL
12-60 mg/dL
HD2 CSF – viral culture
-Adenovirus, Cytomegalovirus, Herpes simplex
virus, Enterovirus, Respiratory syncytial virus,
Varicella –zoster virus, Influenza virus,
Parainfluenza virus
No virus isolated
HD2 CSF – autoimmune Encephalopathy Evaluation
-NMDA-R Ab; VKGKC-complex Ab, GABA-B R Ab,
AMPA-R Ab, ANNA-1, ANNA-2, ANNA-3, AGNA-1,
PCA-1, PCA-Tr, Amphiphysin Ab, CRMP-5-IgG,
ANA
All negative
CSF – Histoplasma Ab, Coccidioides Ab, HSV 1
DNA PCR, HSV 2 DNA PCR, None detected
CSF- VDRL Non reactive
Urine – Trachomatis RNA, Neisseria Gonorrhoeae Not detected
EEG unremarkable
HD1 CT chest, abdomen, pelvis with contrast 1 cm RUL* nodule with minimal central
calcification; otherwise unremarkable CT
scan
Note: follow-up in 3 months to monitor size
HD1 MRI lumbar spine with and without contrast Unremarkable
HD1 MRI thoracic spine with and without contrast Unremarkable
HD1 MRI cervical spine with and without contrast Unremarkable

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Date
Diag
nostic tests
Results
Normal range
HD1 MRI brain with and without contrast Unremarkable
HD2 Echo 2D Normal echo; LVEF* normal (55-60%), RV*
normal size and function
HD1 Hb A1c (normal) 5.1%
HD1 PT, INR PT: 10.2
INR: 1.0 PT: 9.7-11.8
INR: .9-1.2
HD – hospital day; RUL – right upper lobe; LVEF – left ventricular ejection fraction; RV – right ventricle
Given lorazepam for suspected catatonia without improvement
Suspected PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections)
Dc with antibiotics: amoxicillin-clavulanate 875mg-125mg oral tablet; 1 tablet q12 hours & tinidazole 500 mg oral tablet: 1.5 tablets BID
Follow-up appointment with neuropsychiatrist, immunologist
Table 2. Diagnostic testing at the second private hospital
Total hospital days: 21
Date
Diagnostic tests
Results
Normal range
HD*14 IgA <7 82-453 mg/dL
HD14 IgG 1070 751-1560 mg/dL
HD14 IgM 188 46-304 mg/dL
HD14 IgE 5 <114 kU/L
HD2 Total bilirubin mildly elevated 1.3 .1-1.2 mg/dL
HD2 Direct bilirubin mildly elevated .4 <.3mg/dL
HD20 Total bilirubin .7 .1-1.2 mg/dL
HD2 Plasma Ammonia 68 <42mcmol/L
HD20 Plasma ammonia 44 <42mcmol/L
HD2 TSH, Free T4 – normal 1.28, 1.24 TSH: 0.39-4.60
Free T4: 0.93-1,70
HD2 Vitamin B12 1647* 211-911
HD2 Folate 9.5 2.5-22 ng/mL
Vitamin D 25 hydroxy 35.7 20.0-80.0 ng/mL
HD2 LP opening & closing pressure 140mmH20, 100mmH20
CSF glucose, protein, WBC 68,23,0 WBC, 0 RBC
HD2 CSF: Anti-neuronal cell Ab 2.8 0-1.0
CSF anti-RI Ab (paraneoplastic lab testing),
NMDA-R Ab negative

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Date
Diagnostic tests
Results
Normal range
CSF: neuron specific enolase 2.9 <8.9
CSF fungus culture, virus, bacteria; West Nile IgM
& IgG, VDRL, CMV IgG, Toxoplasma IgM & IgG,
HSV PCR, Enterovirus RT PCR
Negative for fungus, virus, bacteria
Negative results/nonreactive
CSF: Lyme Disease Abs, IBL No bands detected
CSF: Cysticercus Ab <0.75 <0.75
CSF ammonia 40 <42mcmol/L
CSF India Ink
negative
CSF: Coccidiomycosis IgM & IgG, Cryptococcus
antigen negative
HD14 Serum Mycoplasma pneumonia antibody IgG 1.92 <=,90
HD14 Serum Mycoplasma pneumonia antibody IgM 587 <770U/mL
HD14 Serum Angiotensin Converting Enzyme 7 9-67 U/L
HD14 Serum B henselae IgG & IgM screen negative
HD14 Serum enterovirus PCR not detected
HD14 Serum Tropheryma whippelli DNA not detected
HD17 Creatine Kinase 48 0-171 U/L
HD2 RPR negative
HD14 FTA-ABS nonreactive
HD2 HIV Ag/Ab combo negative
HD3 HBV core Ab IgM, HCV Ab negative
HD3 HBV surface Ab 110 >12 MIU/MLpost vaccination protection
HD14 Anti neutrophic cytoplasmic Ab (ANCA) <10 <10
HD5 Immune electrophoresis (IEP) Normal pattern, no monoclonal proteins
detected
HD14 Serum protein electrophoresis (PEP) – mildly
elevated Alpha 1, serum & alpha 2 serum; normal
Total protein, albumin, beta, total gamma
Alpha 1: 0.37
Alpha 2: 1.00 Alpha 1: 0.18-0.34G/dL
Alpha 2: 0.43-0.87
HD5 Serum ASO 297 <116 IUM/mL
HD14 CMV DNA PCR 0 <5 copies
HD14 EBV DNA PCR 0 <5 copies
HD14 Quantiferon TB Gold negative
HD14 C-Reactive Protein .9 <5mg/L
HD1 PT 14.2 11.9-14.4sec

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Date
Diagnostic tests
Results
Normal range
HD1 INR 1.0 <3.6
HD1 PTT 46 22-37
HD2 Urine toxicology screen Negative
HD2 Urine analysis Negative
HD1 EKG Prolonged QTc interval
HD7 CSF: NMDAR Ab 1:1, negative 1:1
HD7 Serum: NMDAR <1:10, negative <1:10
HD2 MRI Brain with and without contrast No mass, hemorrhage, or acute infarction. No
evidence of rhomboencephalitis. Mild
cerebellar atrophy
HD2 Chest X-ray Normal exam of the chest
HD2 Abdominal Ultrasound 4.0x4.5x3.8 cm liver mass on left lobe with
internal blood flow
HD3 MRI Abdomen and Pelvis with and without contrast
Liver with exophytic mass measuring
4.9x4.1x4.3cm within the lateral segment left
lobe likely focal nodular hyperplasia
HD3 EEG Mildly abnormal EEG due to presence of very
mild slowing
HD8-9 Continuous Video-EEG monitoring Normal
HD- Hospital day, Tx: 5 doses if IVIG, no clinical effect, Lorazepam: 1 mg q4 hrs injection, Olanzapine 5 mg, Mirtazapine 45 mg, Discharged with, -4 mg of methylprednisolone
-Vita D3, 1000units/ tab, 2 tabs po daily, 60 days, -Megestrol acetate 400 mg BID, 30 days, -Mirtazapine: 45 mg daily

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Table 3. Diagnostic testing at UCI
Total hospital days: 96
Date
Diagnostic tests
Results
Normal range
HD*7 CK 75 30-223
HD7 C-Reactive Protein .2 0-1.0mg/dL
HD9 ANA Screen negative
HD9 Ribosomal Protein P Antibody 1 0-40 AU/mL
HD15
Serum NMDA Ab, IgG
<1:10
<1:10
HD18 Anti ENA Ab 14 0-19 units
HD18 Serum tryptase 3.4 <11.5ng/mL
HD18 Anti Double-Stranded DNA and ANCA screen negative
HD65 Lupus Sens aPTT screen 45.7 <48.1
HD65 Lupus anticoagulant DRVVT and HEX test negative
HD31 IgA – low <7 68-378mg/dL
HD31 Anti-TPO antibodies 17 <9 IU/mL
HD31 ANNA-1 (Hu), ANNA-2 (Ri), PCA-1 (Yo) Not detected Note: confirmatory testing will not
be performed
HD31 ASO elevated 400 <200
HD31 Lyme Disease Antibody total - negative .90 >1.09
HD32 TSH 151 0.50-5.00 uIU/mL
HD32 CSF tube 4 Glucose 68, protein 40, clear, 0 RBC, 3
nucleated cells, 90% lymphocytes,
10% monocytes
HD32 CSF bacterial & viral culture No growth, no viruses isolated
HD32 CSF: Lyme titers (Borrelia Burgdorferi Ab, ELISA), VDRL Negative
HD32 CSF: anti-neuronal cell Ab .8 0-1.0 units
HD32 CSF: anti-Neuronal cell antibody 20 0-54 units
HD32 CSF: Paraneoplastic panel: ANNA-1, ANNA-2, ANNA-3, AGNA-
1, PCA-1, PCA-2, PCA-Tr, Amphiphysin Ab, CRMP-5, P/Q-type
Calcium Channel Ab, N-type Calcium Channel Ab, AChR
Ganglionic Neuronal Ab, Neuronal (V-G) K+ Channel Ab
negative
CSF: Striational (striated muscle) Ab – High 1:480 <1:120
HD32 CSF pathology No malignant cells
HD32 Spinal LDH <25 <25 U/L

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Date
Diagnostic tests
Results
Normal range
HD32 Thyroglobulin Ab Negative (note: suboptimal specimen) 0-4,0 IU/MI
HD34 BNP 6 0-100pg/mL
HD34 Troponin <.03 <.03 ng/dL
HD39
Iron Panel: transferrin, Iron, TIBC, Percent Saturation, Ferritin normal
HD62 Vitamin B12 750 180-1241 pg/mL
HD62 Vitamin D 25-hydroxy total 23.5 >30 ng/mL
Admission
Urine analysis
negative
Admission
Comprehensive urine drug screen No drugs detected
Admission
Comprehensive blood drug test: Alcohol Ethyl Not detected
Admission
Blood cultures No growth, no anaerobic growth, no
acid fast bacilli isolated, no fungus
isolated
HD10 MRI Brain with and without contrast Calipers of the ventricles, sulci, basal
cisterns, are prominent for age 25,
including some cerebral atrophy. No
other abnormalities detected
HD15 CT Abdomen/Pelvis with contrast 5.5 cm enhancing mass with central
scar in left liver lobe suggestive of focal
nodular hyperplasia
HD15 CT Chest with contrast Calcified granuloma located on RUL*.
No intrathoracic neoplastic or infectious
process
HD20 MRI Abdomen with & without contrast Liver lesion 5.5x4.3x4.5cm mass
consistent with focal nodular
hyperplasia; no acute abdominal
findings
HD60 MRI Abdomen with & without contrast Stable 5 cm mass in left hepatic lobe
with central scar, consistent with focal
nodular hyperplasia
HD20 Ultrasound of Scrotum/Testicle No focal testicular lesions noted
HD32 Thyroid Sonogram Normal. No focal thyroid nodule or
mass
HD- Hospital day; RUL- right upper lobe

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Table 4. Medication table at UCI
Medication
Date and dosage
Lorazepam Up-titrated: in mg/day: 3 10 16  24  28  32 48 72mg for 3 days. Since patient showed little
improvement, he was tapered off from 72  36 24. Patient had poor PO intake so dose was increased
back up to 36 for 3 days and titrated down  24  12  8  6  4 2  4 up-titrated due to withdrawal
symptoms of poor PO intake  2; patient was discharged with 2 mg TID
Lithium HD* 31: started 600 mg daily PO 900 mg daily; stopped HD 45
Olanzapine
HD 29: started 5 mg daily PO

10 mg daily

30 mg daily; stopped HD 45
Selegiline (transdermal) HD 53: started 6 mg daily patch 12 mg daily patch until HD 96; discharged with 12 mg daily patch
Minocycline HD 81: started 200 mg/day until HD 96; discharged with 200 mg/day
Memantine HD 85: started 5 mg/day 10 mg/day until HD 96; discharged with 10mg/day
ECT Received 9 times starting HD 68
After session #6, patient began speaking in phrases
After session #7, patient was able to recall long-term memories
Busch-Francis Catatonia Assessments:
Before ECT: 32
After ECT #4: 14, 13
After ECT #5 0 and remained 0
Vancomycin/ Piperacillin-Tazobactam Patient developed pneumonia likely secondary to aspiration and completed a 10-day course of antibiotics.
Amphetamine/ Dextroamphetamine HD 89: start 10 mg  20 mg  30 mg
HD- hospital day
Patient was supplemented with thiamine 50mg daily, cholecalciferol 400 IU daily, and fish oil. He was initially given a trial of valproic acid but refused any PO intake at that time
so the drug was discontinued. He was given methylprednisolone 1x for possible autoimmune encephalitis with possible etiologies including post-streptococcal infection related
to autoimmune PANDAS versus post-Lyme infection vs paraneoplastic syndrome; however, it was discontinued

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Functional imaging can provide further evidence
of this. In a study (5), behavioral interventions
showed cerebral activation in executive control
and default mode networks, using functional
magnetic resonance imaging. In a recent meta-
analysis of studies using diffusion tensor imaging
(DTI), there was significant correlations between
long term changes in large tracts and cognition
[19].
In case of Mr. A, the patient was discharged with
partial hospitalization program (PHP) follow up
and psychiatrist appointments to manage his
medications. The ECT treatment was stopped
without immediate deterioration. Two situations
deserve more consideration. First, when the
compliance to medications decreased after
hospitalization, the symptoms of catatonia
started to resurface (mutism, waxy flexibility and
stereotypical behavior) which successfully
remitted with better medication compliance.
Second, when the frequency of the PHP
decreased from five to three days a week due to
insurance considerations, the same scenario re
occurred.
The memory, immediately after the resolution of
most of Mr. A’s catatonia symptoms, was poor,
including his immediate memory as well as his
long-term memory. After initiation of memantine
immediate memory improved within the first
week (he started to remember details of the visits
he just received from friends). Long term memory
continued to improve over the weeks following,
first devoid of emotions, but as time passed by,
at eight weeks he started to recall the fear and
horror of first days of psychiatric hospitalization
when an occasional code was called and knew
he could not initiate any body movements.
4. CONCLUSION
TBI is a common condition and a significant
cause of morbidity and mortality. Catatonia as
result of TBI can present as a very insidious
condition, happening at various intervals from the
date of initial trauma. The complexity of TBI
anatomical variability and the consequences,
both short and long term from the original trauma
can explain sparsity of research in catatonia
secondary to TBI. Therefore, we believe that is
very important to increase physician’s awareness
of this condition in patients with TBI.
CONSENT
All authors declare that ‘written informed consent
was obtained from the patient (or other approved
parties) for publication of this paper and
accompanying images.
ETHICAL APPROVAL
It is not applicable.
COMPETING INTERESTS
Authors have declared that no competing
interests exist.
REFERENCES
1. Baldwin G, Breiding M, Sleet D. Using the
public health model to address
unintentional injuries and TBI: A
perspective from the centers for disease
control and prevention (CDC). Neuro
Rehabilitation. 2016;39(3):345-9.
2. Khalafian A, Dukes C, Tucker P.
Consultation Dilemma catatonia in a
patient with prior TBI: MentaI or medical
disorder? J Okla State Med Assoc.
2015;108(8):358-60.
3. Irimia A, Van Horn JD. Functional
neuroimaging of traumatic brain injury:
Advances and clinical utility.
Neuropsychiatr Dis Treat. 2015;11:2355-
65.
4. Franke LM, Walker WC, Hoke KW, et al.
Distinction in EEG slow oscillations
between chronic mild traumatic brain injury
and PTSD. Int J Psychophysiol. 2016;
106:21-9.
5. Korn A, Golan H, Melamed I, et al. Focal
cortical dysfunction and blood-brain barrier
disruption in patients with postconcussion
syndrome. J Clin Neurophysiol. 2005;
22(1):1-9.
6. Sponheim SR, McGuire KA, Kang SS,
et al. Evidence of disrupted functional
connectivity in the brain after combat-
related blast injury. Neuroimage. 2011;
54 Suppl 1:S21-9.
7. Castellanos NP, Paul N, Ordonez VE,
et al. Reorganization of functional
connectivity as a correlate of cognitive
recovery in acquired brain injury. Brain.
2010;133:2365-81.
8. Sharova EV, Chelyapina MV, Korobkova
EV, et al. [EEG-correlates of
consciousness recovery after traumatic
brain injury]. Zh Vopr Neirokhir Im NN
Burdenko. 2014;78(1):14-25. Discussion
25.

Groysman et al.; BJMMR, 19(4): 1-12, 2017; Article no.BJMMR.30545
12
9. Rommel O, Tegenthoff M, Widdig W, et al.
Organic catatonia following frontal lobe
injury: Response to clozapine. J
Neuropsychiatry Clin Neurosci. 1998;
10(2):237-8.
10. Smith JH, Smith VD, Philbrick KL, et al.
Catatonic disorder due to a general
medical or psychiatric condition. J
Neuropsychiatry Clin Neurosci. 2012;
24(2):198-207.
11. Mann SC, Caroff SN, Bleier HR, et al.
Lethal catatonia. Am J Psychiatry. 1986;
143(11):1374-81.
12. Ghajar J. Brain trauma: Expert Q & A;
2008.
Available:http://www.pbs.org/wgbh/nova/b
ody/ghajar-concussion.html
13. James BO, Omoaregba JO, Lawani AO,
et al. Subdural haematoma presenting as
catatonia in a 20-year-old male: A case
report. Cases J. 2009;2:8032.
14. Woods SW. Catatonia in a patient with
subdural hematomas. Am J Psychiatry.
1980;137(8):983-4.
15. Wilcox JA, Nasrallah HA. Organic factors
in catatonia. Br J Psychiatry. 1986;149:
782-4.
16. Ahuja N. Organic catatonia: A review.
Indian J Psychiatry. 2000;42(4):327-46.
17. Hesslinger B, Walden J, Normann C.
Acute and long-term treatment of catatonia
with risperidone. Pharmacopsychiatry.
2001;34(1):25-6.
18. Alisky JM. Minimally-responsive head
injury survivors may have chronic catatonia
reversed years after an accident.
Singapore Med J. 2009;50(11):1117-8.
19. Roberts RM, Mathias JL, Rose SE.
Relationship between diffusion tensor
imaging (DTI) findings and cognition
following pediatric TBI: A meta-analytic
review. Dev Neuropsychol. 2016;41(3):
176-200.
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