Research Connect

Hiremath, Vijaykumar

Pogula, Dr. Anusha

M, Dr. Kishor

Digital Journal of Clinical Medicine 
Volume 3 Issue 3 Article 9 
1-1-2021 
Case of severe depression with psychotic symptoms in childhood 
Vijaykumar Hiremath 
JSS AHER 
Dr. Anusha Pogula 
JSS AHER 
Dr. Kishor M 
JSS AHER 
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Recommended Citation 
Hiremath, Vijaykumar; Pogula, Dr. Anusha; and M, Dr. Kishor (2021) "Case of severe depression with 
psychotic symptoms in childhood," Digital Journal of Clinical Medicine: Vol. 3: Iss. 3, Article 9. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
Case of severe depression with psychotic symptoms in childhood 
Vijaykumar Hiremath Clinical Psychology Resident, Dr. Anusha Pogula PG Psychiatry 
Resident, Dr M Kishor Associate Professor Of Psychiatry JSS MC & Hospital, JSSAHER , 
Mysore  
 
CLINICAL HISTORY: 
A 13yr old boy, studying in 8th grade was brought by his parents to the psychiatry outpatient 
department with chief complaints of not sleeping, decreased interaction with family members 
and friends, declining to eat food since 15 days, worsening since 4 days. Parents reported that 
2 months ago his paternal grandmother’s sister committed suicide by hanging at her house. 
Although the boy had neither witnessed the death nor was close to her, he was involved in the 
family rituals including lighting fire to the body as per tradition.  
After a few days of the funeral, he reported fear of going to the fields where the cremation 
was done and wouldn’t go out and play. He was later taken to temples and reported little 
improvement from fear following the prayers and pooja.   
20 days later, the patient had an episode of fever. They consulted a doctor in a local clinic and 
reported recovery within a day of taking medication.   
15 days ago, parents reported that while playing cricket, he had accidentally stepped into an 
ant hill which was considered holy. After that he reported fearfulness, that he was seeing 
images of his dead relative, and that she was calling him, and that he also might die. He also 
complained of breathlessness and chest discomfort. Parents had tried to counsel him and calm 
him down. Next day, they consulted a local doctor for mild fever, and he recovered within a 
day but reported a rash and itching over the hands and thighs which was relieved on further 
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medication, it was diagnosed as a drug reaction.Patient was on tab.cefixime, 200mg twice a 
day. He was again taken to a temple and performed pooja and was sent to his maternal 
grandmother’s house where he continued to report fearfulness and over the next few 
days, parents noticed dullness in his activities such as not attending his online classes, not 
having food ,not sleeping enough as before.   
After returning home, he was not talking to anyone, more so with friends & neighbours, with 
whom he would generally interact before. He was found staring at the wall most of the time. 
And thus, reported to hospital. There was no history of death wishes or suicide attempt.   
Treatment History  
Medical History: No history of previous medical illness.  
Psychiatry History: No history of previous psychiatry illness.   
Paediatrician and neurology opinion reported no abnormalities.  
Family History: Bipolar affective disorder in mother (currently in remission) and paternal 
aunt. Alcohol use disorder in father. IDD (intellectual developmental disability) in maternal 
aunt. Epilepsy in his elder sister.  
 
EXAMINATION AND INVESTIGATIONS: 
The boy moderately built and nourished. Conscious, oriented, not cooperative  
Vitals -stable  
Systemic examination: CVS: S1 S2 normal,no murmurs  
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 RS: b/l normal vesicular breath sounds. no added sounds.  P/A: soft,non tender, bowel 
sounds plus.  
 CNS: no abnormality detected.  
Mental status examination: {kirby’s method for uncooperative patients} 1)General reaction 
and posture:  
Attitude: not cooperative, unable to maintain postures.  
2)Facial expressions: no emotions displayed, staring blank expressions 3)Eyes open not 
following hand movements 
Decreased blinking.  
4)Muscular reactions: normal  
5)Emotional responsiveness- not responsive  
6)Speech- could not be assessed  
7)Writing-not cooperative  
Assessment:  
Children’s depression rating scale (CDRS) and was found that he had a severe depressed 
mood.   
Patient had scored 30 in Brief Psychiatric Rating Scale (BPRS) in which the scores were 
severe in Emotional withdrawal(6), Depressive mood(6), Uncooperativeness(6), and blunted 
affect(6), moderate in Motor retardation(4), very mild in mannerism and posturing(2).  
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MRI BRAIN to rule out organic pathology (as he had an episode of fever and? medication 
induced rash) reported to be within normal limits.  
 
FINAL DIAGNOSIS: 
According to WHO ICD 10: Severe depression with mood congruent psychotic symptoms.  
Severe depressive episode with psychotic symptoms:  
Episode which meets the criteria of severe depression and in which delusions or 
hallucinations, or depressive stupor are present. Auditory hallucinations are usually of 
defamatory or accusatory voices or olfactory delusions of rotting filth or decomposing flesh. 
Severe psychomotor retardation may progress to stupor. If required,delusions or 
hallucinations may be specified as mood-congruent or mood-incongruent.  
 
DISCUSSION:  
Treatment:  Patient was admitted for inpatient care. 
● started on Antipsychotic (Serotonin Dopamine Antagonist) Tab Resperidone 1mg 0-0-1.  
● Antidepressants SSRI Tab Sertraline 50mg 1-0-0  
● Anxiolytic Benzodiazepine Tab Clonazepam 0.25mg SOS.  
Patient’s family members were educated. Supportive psychotherapy was initiated. Patients 
improved with these medications and hence discharged with these medications. 
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Depression is the most common psychiatric disorder, with more than 350 million people 
affected worldwide. Depression among children presents with atypical features with 
symptoms such as increased sleep, irritability, increased appetite unlike adults who present 
with poor sleep, low mood and reduced appetite. Hence Children with depression should be 
evaluated comprehensively. This case of depression in childhood with psychotic symptoms ( 
of auditory hallucinations & severe psychomotor retardation) particularly with family history 
of bipolar disorder, highlights atypical presentation of mood disorder in children. The 
psychotic symptoms in childhood depression are rare and in this case because of coincidental 
fever, organic causes had been ruled out with brain imaging. As there were no features of 
infections or inflammation were present in investigation, a diagnosis of Depression was 
considered. The Prevalence of Depressive Episode & Recurrent Depressive Disorder in 
adolescents is 0.8 %(0.3 – 1.4) [1] Prevalence of Bipolar affective disorder in adolescents is 
0.6% (0.1 to 1) [1]  
The Risk of Bipolar Disorder (BPAD) when one parent has bipolar disorder is 15-25% [2] 
And Risk of BPAD when a second degree relative has BPAD is 3-4 % [2]. It is important to 
identify early symptoms and manage for prevention of severe impact on the childhood. There 
are higher chances that this case may present with Bipolar Disorder or schizophrenia over the 
course of life considering the high degree BPAD among family members. Childhood 
psychotic symptoms have also been considered as subclinical phenotype of schizophrenia in 
ecological research.[3]  
 
ACKNOWLEDGEMENTS:  None  
 
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Hiremath et al.: Case of severe depression with psychotic symptoms in childhood
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REFERENCES:  
1) Gururaj G. VM. National Mental Health Survey of India, 2015-16 Prevalence, Pattern and 
Outcomes. NImhans Rep 2015-16 [Internet]. 2016;(May 2018):1–198. Available from: 
National Mental Health Survey of India, 2015-16 National Mental Health Survey of India, 
2015-16 .  
2) Mattes JA. Bipolar disorder? Arch Gen Psychiatry. 2010;67(11):1198. 
3) Fisher HL, Caspi A, Poulton R, Meier MH, Houts R, Harrington H, et al. Specificity of 
childhood psychotic symptoms for predicting schizophrenia by 38 years of age: A birth 
cohort study. Psychol Med. 2013;43(10):2077–86. 
 
 
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English

Case of severe depression with psychotic symptoms in childhood

Moudgalya, Abhigna S, Dr

Patil, Vikram, Dr

JSS Academy of Higher Education and Research 
Research Connect 
Radiology Teaching Files 
2021 
Post primary pulmonary tuberculosis: A case report 
Abhigna S. Moudgalya Dr 
JSS Medical College, JSSAHER 
Vikram Patil Dr 
JSS Medical College, JSSAHER, caihs@jssuni.edu.in 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Moudgalya, Abhigna S. Dr and Patil, Vikram Dr, "Post primary pulmonary tuberculosis: A case report" 
(2021). Radiology Teaching Files. 5. 
https://rescon.jssuni.edu.in/radiologyteachingfiles/5 
This Chest Imaging is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Radiology Teaching Files by an authorized administrator of Research Connect. 
Post primary pulmonary tuberculosis: A case report. 
 
CLINICAL HISTORY:  
Patient presented with a mild cough and progressive hemoptysis since 10 days. Loss of appetite 
and loss of weight from past 6 months was noted. A past history of untreated cough with mild 
sputum was also recognized.  
ZN staining: Positive for acid fast bacilli 2+ 
KOH preparation: Negative for fungal elements. 
CBNAAT: Positive for MTB. 
 
IMAGING FINDINGS 
 
Chest X-ray PA view:  
 
Fig 1: Well defined thick walled cavitatory lesion in the right upper zone with adjacent 
bronchiectatic changes . Volume loss of the right upper lobe with mild rightward tracheal shift, 
superior retraction of hilum and crowding of vessels and ribs. Non homogeneous and 
reticulonodular opacities noted in bilateral lungs predominantly in the right. 
 
 
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HRCT thorax: 
 
Fig 2: Multiple centrilobular nodules with tree in bud opacities noted in bilateral lungs 
predominantly in the right.  
 
Fig 3: Patchy areas of consolidation in bilateral lungs predominantly in the right upper lobe.  
 
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Fig 4,5: Prone imaging. 
Fig 4, Fig 5: Volume loss in the upper lobe of the right lung. Thick walled irregular 
fibrocavitatory lesion measuring 6.0 x 4.8 x 4.5cm (AP x TR x CC) in apical segment of right 
upper lobe. Areas of breakdown with central soft tissue density within the cavitation (with no 
change in position on prone imaging).  
 
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Fig 6: Tractional bronchiectasis and regional thickening of the pleura.  
 
 
Fig 7: Few enlarged lymph nodes in pretracheal, paratracheal, prevascular, precarinal and 
subcarinal regions.  
DIFFERENTIAL DIAGNOSIS: 
• Post-primary tuberculosis. 
• Chronic fungal infection with exacerbation- Aspergillosis. 
• Bronchogenic Carcinoma. 
 
FINAL DIAGNOSIS: 
● Post-primary tuberculosis with reactivation. 
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DISCUSSION : 
Pulmonary tuberculosis (TB) is a common worldwide infection and a medical and social 
problem causing high mortality and morbidity, especially in developing countries. 
The traditional imaging concept of primary and reactivation TB has been recently challenged and 
radiologic features depend on the level of host immunity rather than the elapsed time after the 
infection.¹ With regard to post-primary tuberculosis, evidence suggests that patients in endemic 
areas are more likely to be infected by a second strain of tuberculosis than to experience 
reactivation of a previously infected strain.² 
 
 
Plain radiograph:  
● Airspace consolidation, cavities, fibrosis, retraction, distortion, endobronchial spread to 
dependent lung, acinar nodular opacities 
● Apical and apical posterior segments of upper lobes and superior segments of lower 
lobes.  
 
CT Findings:   
● Morphology2 
o Consolidation (100%) 
▪ Lobular and peribronchial 
o Cavitation (50%)  
▪ Wall thickness variable: Thick > thin, shape may be irregular. 
▪ Air-fluid levels are uncommon. 
▪ Often surrounded by consolidated lung. 
o Endobronchial spread 
▪ Nodules: Centrilobular rosettes (acinar), poorly defined, 2-10 mm in size 
▪ Tree-in-bud appearance. 
▪ Bronchial wall thickening. 
o Volume loss in affected lung 
▪ Usually from fibrosis (30%): Architectural distortion, bronchiectasis, 
emphysema. 
● Distribution 1 
o Often segmental in distribution 
o Apical and posterior segments of upper lobes, superior segments of lower lobes 
o Bronchogenic spread: Gravity dependent lobes 
● Adenopathy (30%) 
o Classic appearance: Low-density center with peripheral rim enhancement 
o Mean size 3 cm in diameter 
● Pleural effusions (20%) 
o Usually small.  
o Consider complicating bronchopleural fistula. 
o Pleural thickening common in advanced cavitary disease 
● Evolution 
o With successful treatment, consolidation and nodules will resolve, usually over 9-
12 months 
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▪ Signs of fibrosis may increase with increasing volume loss in affected 
lung 
o Calcification in lung (Ghon lesion) and lymph nodes (Ranke complex) may be 
from previous primary disease. 
● Active versus inactive disease 2  
o Activity 
▪ Signs of endobronchial spread 
▪ Cavitation 
▪ Consolidation 
o Inactivity 
▪ Requires stability over 6 months. 
 
 
PET:  PET scans using 18F-FDG or 11C-choline can help differentiate tuberculous granuloma 
from lung malignancy. 1 
 
Treatment: Respiratory isolation for cavitary disease or grossly positive sputum smear until 
antibiotics are instituted. Antituberculous drugs are to be administered depending on the 
sensitivity.  
Bronchial artery embolization or surgery is required for hemoptysis. Bronchial and nonbronchial 
systemic arteries are the main source of bleeding and are embolized with polyvinyl alcohol 
particles or gelatin sponge. Immediate cessation of bleeding occurs in more than 75% of patients; 
however, long-term recurrences are common in patients with progressive disease. 3  
In cases of chronic infection, surgical resection may become necessary. 
 
 
REFERENCES: 
 
1. Jeong YJ, Lee KS. Pulmonary tuberculosis: up-to-date imaging and management. American 
Journal of Roentgenology. 2008 Sep;191(3):834-44. 
2. Nachiappan AC, Rahbar K, Shi X, Guy ES, Mortani Barbosa Jr EJ, Shroff GS, Ocazionez D, 
Schlesinger AE, Katz SI, Hammer MM. Pulmonary tuberculosis: role of radiology in diagnosis 
and management. Radiographics. 2017 Jan;37(1):52-72. 
3. Kalva SP. Bronchial artery embolization. Techniques in vascular and interventional radiology. 
2009 Jun 1;12(2):130-8. 
 
 
 
 
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Post primary pulmonary tuberculosis: A case report

Tapadar, Sourav

Tapadar, Dr. Sharmila

Digital Journal of Clinical Medicine 
Volume 3 Issue 2 Article 7 
1-1-2021 
A Case Of Mucinous Cystadenocarcinoma of Ovary In A 13 Year 
Old Female 
Sourav Tapadar 
JSS AHER 
Dr. Sharmila Tapadar 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Tapadar, Sourav and Tapadar, Dr. Sharmila (2021) "A Case Of Mucinous Cystadenocarcinoma of Ovary In 
A 13 Year Old Female," Digital Journal of Clinical Medicine: Vol. 3: Iss. 2, Article 7. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case of Mucinous Cystadenocarcinoma of Ovary In A 13 Year Old Female 
Sourav Tapadar 7th Term MBBS  
Dr. Sharmila Tapadar, JSS Medical College, JSS AHER,Mysuru 
CLINICAL HISTORY  
A 13-year-old nulliparous unmarried female patient hailing from Lucknow presented with 
non-specific complaints of gaseous distension of abdomen, nausea, and abdominal pain since 
the past 2 months. There is a history of constipation for the last 1 month which is relieved by 
laxatives. The consistency, as well as the color of the stools, is normal. The patient also 
complains of a lump felt in the lower abdomen for the past 1 month which increased in size in 
the past 1 week. The size of the lump does not vary with cough, posture, or strain.  
Negative History 
▪ No h/o trauma prior to the swelling 
▪ No h/o abnormal menstrual flow 
▪ No h/o significant weight loss or weight gain  
▪ No h/o urinary symptoms 
▪ No h/o similar complaints in the family 
▪ No h/o past surgeries 
▪ No h/o use of any contraceptives 
Obstetric History 
Nulliparous 
Age of menarche=13 years 
Duration= 5 days/30 
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Tapadar and Tapadar: A Case Of Mucinous Cystadenocarcinoma of Ovary In A 13 Year Old F
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Frequency of cycle= 29 days  
No of pads= 2-3/day 
Normal flow with no associated pain & clots 
EXAMINATION AND INVESTIGATIONS: 
General Physical Examination 
The patient was alert, conscious, cooperative, and well oriented to time, place, and person. 
She was moderately built and well-nourished. 
Pallor + 
No Icterus 
No cyanosis 
No clubbing 
No lymphadenopathy 
No edema 
Systemic Examination 
Per Abdomen- On inspection & palpation,  
Elliptical shaped lump in the right iliac fossa measuring 12×15 cm. The margins are not 
appreciable. The overlying skin is normal. The size doesn’t increase on cough or strain. No 
tenderness No pulsatility Compressibility or reducibility is absent. Cystic in consistency 
Per Vaginal Examination- On inspection and palpation, vulva is normal. Vaginal walls are 
normal on  
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specular inspection and palpation. CVS- S1, S2 heard. No murmur 
RS- B/L Normal vesicular breath sounds, no added sounds 
Blood investigations 
Hb: 10.70 gm/dl 
TLC: 16,200 cells/mm3 
Platelet: 6,86,000 cells/mm3 
RBC: 3,13,000cells/mm3 
MCV- 79.60 fl 
MCH- 25.70 Pg 
MCHC- 32.20g/dl 
RDW-CV- 17.2% 
HS CRP- 22.3 mg/L 
AFP= 2 IU/ml 
Beta HCG= 0.40 mIu/ml 
Serum CA-125= 90.9U/ml 
Serum CEA= 1.78 ng/ml 
CT Scan 
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Tapadar and Tapadar: A Case Of Mucinous Cystadenocarcinoma of Ovary In A 13 Year Old F
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A large well-defined space-occupying lesion of size 30x12x10 cm is noted in the left 
hypochondrium, left lumbar and left iliac fossa region and seen crossing the midline. The 
solid portion of the SOL shows the presence of calcification & heterogeneous enhancement 
patterns. Multiple rounded cystic spaces are noted. No significant organ infiltration was 
noted. 
Small bowel loops are displaced to the left side & the uterus is displaced to the right side.  
USG of whole abdomen 
A large well defined rounded multiseptated, thick-walled cystic fluid collection/space-
occupying lesion of size 19.46 x 20.34 x 19.61 cm & volume 4064 ml is noted filling the 
entire peritoneal cavity. The cystic space appears clear with few showing bright internal 
echoes. 
Histopathological Examination 
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Papillary fronds lined by cuboidal to columnar cells with areas of pseudostratification. 
Individual cells have increased nuclear cytoplasmic ratio and are vesicular to hyperchromatic 
nuclei. The cells also have intracytoplasmic mucin. Mitotic activity is noted.  
 
FINAL DIAGNOSIS 
Stage II U/L mucinous cystadenocarcinoma of the left ovary. 
DISCUSSION 
 
Ovarian tumors are broadly classified into 3 types: 
▪ Epithelial cell tumors 
▪ Germ cell tumors 
▪ Sex cord tumors 
Epithelial cell tumors are the most common ovarian tumors overall. In adolescent females, 
germ cell tumors are most commonly seen. Majority of the ovarian tumors in such an age 
group are non neoplastic. Therefore, germ cell tumors are usually suspected as the first 
differential diagnosis in such a patient. Tumor markers are used as part of the preoperative 
investigation for differential diagnosis in most cases, but they may be important to monitor 
postoperatively for complete resection of the mass, as well as relapse. CA-125 has the 
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potential to identify epithelial cell tumors while AFP & HCG levels help in identifying Germ 
Cell Tumors.(Ref 1) In this patient, AFP & HCG levels are normal which are usually 
elevated in GCTs. Instead, CA-125 levels are elevated which makes us suspect a case of 
epithelial cell tumor of the ovary. Data shows that the cases of epithelial cell tumors under 20 
years of age  are reported in 17% of cases of which only 25% are malignant. (Ref 2) 
Epithelial cell tumors are usually b/l and non-malignant  in the majority of cases. (Ref 3) 
However, in this patient it is u/l and malignant. Surgery is implicated immediately in this 
case.  
Management of ovarian cysts depends on the patient’s age, size of the cyst, surface invasion 
and its histo-pathological nature. Conservative surgery as ovarian cystectomy and salpingo-
oophorectomy is adequate for benign lesions. However, if there is any sign of malignancy 
and depending on the stage of the tumor, hysterectomy and debulking surgery along with 
chemotherapy may also be required. In post menopausal females where this tumor is most 
commonly seen, debulking surgery with hysterectomy is preferred. 
Since this is a case of an adolescent patient, debulking surgery is avoided. 
Total Abdominal Hysterectomy with Bilateral Salpingo Oophorectomy is implicated in stage 
1 & 2 tumors while Debulking surgery in stage 3 & 4 followed by chemotherapy. (Ref 4) 
In our case, although the tumour was removed completely and intact with the affected ovary, 
our patient was given appointments for 4 cycles of chemotherapy every 3 months for a year. 
CA-125 level is constantly monitored during this period since there is a chance of recurrence 
of such a tumor. 
  
ACKNOWLEDGEMENTS : None 
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REFERENCES: 
1. Remah M Kamel. A massive Ovarian Cystadenoma. Department of Obstetrics & 
Gynecology, Faculty of Medicine, Jazan University. December 18, 2009: 3-5 
2. Manoj R Somagutta, Enkhmaa Luvsanyam, Molly S. Jain, Krystel Elliot Thieberge, Amit S. 
Grewal, Siva K Pendyala, Charles Edwards. A Rare Case of Massive Ovarian Mucinous 
Cystadenoma With Postmenopausal Bleeding. Cureus. September 02, 2020: 1-2 
3. Şenol Biçer, Zehra Erkul, Necla Peker. A 9-kg Ovarian Mucinous Cystadenoma in a 14-
Year-Old Premenarchal Girl. Department of Pediatric Surgery, Erzincan University, Medical 
School, Erzincan, Turkey. April 22, 2014: 3-7 
4. Baohong Gu, Xuemei Li, Zedong Feng, Yang Yu, Bofang Wang, Maswikiti Ewetse Paul, 
Hao Chen. A Huge Ovarian Mucinous Cystadenoma in a 15-Year-Old Girl with Situs 
Inversus Totalis: Report of a Rare Case. July 18, 2020: 2-5 
 
 
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A Case Of Mucinous Cystadenocarcinoma of Ovary In A 13 Year Old Female

K.N, Dr. Gayathri

Prasad S, Dr. Rajendra

Y.S, Dr. Ravikumar

T, Dr.Varsha

Digital Journal of Clinical Medicine 
Volume 3 Issue 1 Article 10 
1-1-2021 
A Case of Superior Venacaval (Svc) Syndrome 
Dr. Gayathri K.N 
JSS AHER 
Dr. Rajendra Prasad S 
JSS AHER 
Dr. Ravikumar Y.S 
JSS AHER 
Dr.Varsha T 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
K.N, Dr. Gayathri; Prasad S, Dr. Rajendra; Y.S, Dr. Ravikumar; and T, Dr.Varsha (2021) "A Case of Superior 
Venacaval (Svc) Syndrome," Digital Journal of Clinical Medicine: Vol. 3: Iss. 1, Article 10. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case of Superior Venacaval (Svc) Syndrome 
Dr. Gayathri. K.N, Dr. Rajendra Prasad S, Dr. Ravikumar Y.S , Dr.Varsha, Dr.Mariyam ,JSS 
Medical College,JSS AHER,Mysuru  
 
CLINICAL HISTORY: 
An 85year old male patient who is a known case of type 2 diabetes and hypertension and 
COPD on medication came with the complaints of Easy fatigability since 2 months. Cough 
since 30 days , Reduced appetite since 30 days. Giddiness since 7 days. Facial puffiness since 
1 day. 
The patient developed cough associated with expectoration which was whitish, scanty in 
amount, and non-blood tinged, and non-foul smelling since 30 days.  He developed increased 
breathlessness since 20 days. 
No history of fever, chest pain/palpitations. No history of orthopnea/ PND. No history of 
syncope, pain abdomen, decreased urinary output.No history of pedal edema. No h/o 
exposure to covid patient or trauma 
Past history 
No history of thyroid disorders, cardiac disorders 
 
 
EXAMINATION AND INVESTIGATIONS: 
GENERAL PHYSICAL EXAMINATION: 
Afebrile- 97.6’F 
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Bilateral supraclavicular lymph nodes are palpable, hard in consistency, discrete, adherent to 
deeper structures, largest measuring 4x4cms. 
Pallor and icterus present 
Puffiness of face was present 
JVP-  raised; non-pulsatile neck veins 
RS:   
On percussion dullness present over areas on the  right side 
 Right-sided air entry is reduced with crepts present over the right infrascapular, infra 
axillary, and interscapular area. 
 Bilateral ronchi+ 
PER ABDOMEN: 
All findings within normal limits 
CVS: S1, S2 heard. No murmurs. 
CNS: Intact. 
 
BLOOD INVESTIGATIONS: 
Hb:14.5gms/dl 
Total Count: 
15,020/ml 
N:84.4%, L:11.2% 
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RBC:4.75 million/ml 
MCV:87.8fl 
MCH:30.5pg 
MCHC:34.8g/dl 
RDW-CV:12.8% 
PLATELET:4.95lakhs/ml 
PERIPHERAL BLOOD SMEAR: 
Red blood cells are normocytic normochromic. White blood cells are increased in number 
with an increase in neutrophils. Platelets are increased in number. 
Impression: Neutrophilic leukocytosis with thrombocytosis 
URINE MICROSCOPY: 
Plenty of pus cells 
GRAM STAIN OF SPUTUM –Gram-positive cocci in pairs and chains 
CHEST XRAY 
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K.N et al.: A Case of Superior Venacaval (Svc) Syndrome
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Chest x-ray showing right-sided homogenous opacity suggestive of infiltrating 
mediastinal mass over the right side of the chest. 
KOH- preparation of sputum: Budding yeast seen. 
 
FNAC of right supraclavicular lymph node 
                  
 
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FINAL DIAGNOSIS: 
Bronchogenic Carcinoma with Metastasis presenting with SVC Syndrome 
Type 2 Diabetes Mellitus (Newly detected) 
Hypertension COPD 
 
DISCUSSION:  
Superior Vencaval Syndrome (SVC) is the obstruction of superior vena cava, the most 
common etiology being malignancy. It is the obstruction of superior vena cava by primary or 
metastatic cancer (mostly intrathoracic); through invasion, external compression, or 
thrombosis. 
In an article by Straka C et al, it is stated that   The Superior vena cava is thin-walled and is 
opened by relatively low venous pressure, hence making it particularly susceptible to 
compression by adjacent masses. 
The severity and rapidity of onset of symptoms depend on the rate at which the SVC is 
occluded and if collateral venous drainage to develop in time. In the event of SVC 
obstruction, venous pressure in collateral vessels increases and, over time, a collateral 
blood-flow network develops Different vessels may enlarge in response such as the azygos, 
the hemiazygos, intercostal, mediastinal, paravertebral, thoracoepigastric, internal mammary, 
anterior chest wall veins, and thoracoacromioclavicular veins. The azygos vein may connect 
the SVC and the inferior vena cava (IVC) directly, so SVC obstructions that occur below the 
insertion of the azygos vein result in more severe symptoms of  SVC Syndrome[1]. 
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Lung cancer, lymphoma, thymic neoplasms, germ cell tumors, mesothelioma, and other solid 
tumors that cause mediastinal involvement are the commonest[2]. 
Symptoms can range from interstitial edema of the head and neck which are asymptomatic to 
life-threatening complications such as airway narrowing from the upper airway or laryngeal 
edema and cerebral herniation and ischemia secondary to cerebral edema as a result of 
venous outflow obstruction. 
Facial plethora, cyanosis, and arm edema are often observed. A physical examination can 
present as venous collaterals on the chest and neck. Stridor headaches or confusion is also 
present[3]. 
Management of SVC syndrome depends on the presentation and underlying malignancy. 
Patients presenting with stridor from laryngeal edema and stupor from cerebral edema need 
emergent management like with radiation and or stent placement. Upfront radiation before 
histologic diagnosis in stable patients can obscure a pathologic diagnosis and should not be 
pursued. Steroids have a role in steroid-responsive tumors such as lymphoma and thymoma. 
It can control edema in case of airway obstruction. They have not been systematically studied 
for its use in stenting[1]. 
Chemotherapy is the treatment of choice for patients with cancers such as Small-cell Lung 
Carcinoma (SCLC),  lymphoma, and germ cell tumors. 
For SVC Syndrome caused by an infectious etiology, antibiotics should be the first line of 
treatment. In cases of thrombus-driven SVC Syndrome, Anticoagulants are indicated[1]. 
Stent placement and radiotherapy may be required with less chemo responsive tumors such as 
Non-Small Cell Carcinoma(NSCLC)  
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  Surgical repair via bypass grafting with the femoral vein, spiral saphenous vein, Dacron 
graft, or polytetrafluoroethylene graft can put the SVC obstruction in check. However, this is 
mostly used for cases where recanalization via endovascular repair is impossible or has 
failed.   
  Recently, Stereotactic body radiation therapy (SBRT) has become a well-accepted modality 
for administering radiation at a variety of anatomical sites. Potential benefits of SBRT 
include a novel bio-the 
the logic rationale for tumor cell kills as well as a decreased number of treatments, resulting 
in minimized damage to healthy tissue and also decreased treatment cost. It is not an ideal 
treatment method for a patient who needs 
rapid symptom palliation[1]. However Endovascular therapy now acts as a first-line treatment 
for SVC syndrome[3]. 
 
 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
 
1.Straka C, Ying J, Kong FM, Willey CD, Kaminski J, Kim DN. Review of evolving 
etiologies, implications and treatment strategies for the superior vena cava syndrome. 
Springerplus. 2016 Dec 1;5(1):229 
2.Santra A, Nandi S, Mondal S, Chakraborty S. Superior vena cava syndrome due to 
thrombosis: a rare paraneoplastic presentation of bronchogenic carcinoma. Iranian journal of 
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medical sciences. 2016 Jul;41(4):354   3.Hinton J, Cerra-Franco A, Shiue K, Shea L, Aaron 
V, Billows G, Al-Hader A, Lautenschlaeger T. Superior vena cava syndrome in a patient with 
locally advanced lung cancer with good response to definitive chemoradiation: a case report. 
Journal of medical case reports. 2018 Dec;12(1):1-6   
 
Image Courtesy:  In Seminars in interventional radiology 2017 Dec (Vol. 34, No. 4, p. 398). 
Thieme Medical Publishers. Journal of Cytology/Indian Academy of Cytologists 2010 Jan. 
 
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A Case of Superior Venacaval (Svc) Syndrome

Nagaraj, Dr. Punitha

M, Dr. Poornima

Digital Journal of Clinical Medicine 
Volume 3 Issue 2 Article 12 
1-1-2021 
A Case Of P2L2 With Scar Endometriosis With Previous Two LSCS 
Dr. Punitha Nagaraj 
JSS AHER 
Dr. Poornima M 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
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Recommended Citation 
Nagaraj, Dr. Punitha and M, Dr. Poornima (2021) "A Case Of P2L2 With Scar Endometriosis With Previous 
Two LSCS," Digital Journal of Clinical Medicine: Vol. 3: Iss. 2, Article 12. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case of P2L2 With Scar Endometriosis With Previous Two LSCS 
 Dr. Punitha Nagaraj, Dr. Poornima (Associate Professor, Department Of Obstetrics And 
Gynaecology, JSS Hospital), JSS Medical College, JSS AHER,Mysuru  
 
Clinical History  
CHIEF COMPLAINTS: 
27year old P2 L2 came with h/o pain abdomen on and off since 7years, increased since 2 
months. 
HISTORY OF PRESENTING ILLNESS: 
27year old para 2 living 2 came with pain abdomen since 7years, increased since 2months, 
sudden in onset, progressive in nature, pain over suprapubic region, pricking kind of pain, 
aggravates significantly during menstrual cycles and relives after taking medications. Pain 
associated with the mass. Mass present over the cesarean scar , tender in nature , protrudes 
during menstrual cycles. 
NEGATIVE HISTORY: 
No history of menorrhagia 
No history of intermittent bleeding No history of abdominal distension No history burning 
micturition 
No history of increased frequency of micturition No history of constipation 
No history of loss of appetite No history of loss of weight 
No history of twinning and congenital Anomalies 
MENSTRUAL HISTORY : LMP : 20/11/2020 
Past cycles : 3-4 days/30days , 2-3 pads per day , pain ++, no clots 
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OBSTETRIC HISTORY : PARA 2 LIVING 2 , 2FTLSCS 
1st- conceived spontaneously , FTLSCS, male baby, at present 7years alive, healthy 
2nd- conceived spontaneously, FTLSCS, male , at present 4years alive and healthy 
MEDICAL HISTORY : 
no history of Diabetes, Hypertension , Tuberculosis, seizures, bronchial asthma 
PAST SURGICAL HISTORY: 
Underwent open appendectomy 10years back Underwent open cholecystectomy 10years back 
Underwent 2 LSCS 7 and 4 years back with concurrent tubal sterilisation Family history : 
nothing significant 
Personal history : diet mixed , normal appetite, regular bowel and bladder , sleep not 
disturbed 
EXAMINATION AND INVESTIGATIONS 
General physical examination: 
Patient aged 27years , moderately built , moderately nourished , oriented to time, place, 
person. 
No pallor, Icterus , cyanosis, clubbing, lymphadenopathy, Edema 
VITALS: PULSE- 90/MIN 
Blood pressure – 130/80mmhg 
SYSTEMIC EXAMINATION: 
Per abdomen 
Inspection – Abdomen scaphoid shaped 
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All quadrants moves equally on respiration Multiple healed scars present 
1. Right hypochondriac region 10cm healed scar,suggestive of cholecystectomy healed by 
primary intention. 
2. Suprapubic transverse healed scar suggestive of cesarean section healed by primary intention. 
3. 3*3cm circular scar with black pigmentation in subumblical region. 
No dilated veins, all hernial orifices normal 
Palpation : Soft 
No local rise of temperature 
Tenderness present 
3*3cm circular hard mass with black pigmentation in subumbilical region, tender with 
restricted mobility and felt arising from skin to deep down. 
No fluctuant 
No organomegaly 
No Other mass palpable Percussion : tympanic notes in all 9 quadrants Auscultation: bowel 
sounds heard 
Local examination :External genitalia normal 
No excoriation No discharge 
Per speculum : Cervix and vagina normal 
No discharge 
Per vaginal examination: cervix firm , directed downwards backwards, Uterus normal size, 
anteverted. Fornices free and non tender 
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Cvs: s1 s2 heard . No murmurs 
Rs: B/L normal vesicular breath sounds heard. No added sounds Cns: normal 
 
*USG abdomen: well defined subcutaneous hypoechoic lesion 3*2.5cm in lower abdomen at 
incision site. Showing increased vascularity. 
 
Subcutaneous scar endometriosis. 
DIAGNOSIS 
Final Diagnosis: 
P2L2 with scar endometriosis with previous 2 LSCS 
DISCUSSION 
Endometriosis is a benign disease, defined as presence of ectopic (outside the uterus ) 
endometrial gland and stroma. 
Risk factors: 
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Previous LSCS /late marriages/ late child birth / genital tract obstruction / frequent and 
prolonged menstrual cycles / nulliparity / early menarche 
Theories of sites of endometriosis: 1. Pelvic endometriosis- Retrograde metaplasia 
2. Abdominal viscera – coelomic metaplasia 3.Pelvic peritoneum- coelomic metaplasia 
4.Rectovaginal septum – coelomic metaplasia 5.umbilicus – coelomic metaplasia 
6. Abdomen scar – direct implantation 
7. Episiotomy scar – direct implantation 
8. Vagina and cervix – direct implantation 
9. Lymph nodes – Lymphatic spread 
10. Other- vascular genetic immunologic 
SCAR ENDOMETRIOSIS 
Scar endometriosis is a rare entity reported in gynaecology literature and presents in women 
who has undergone previous abdomen or pelvic surgeries . It is defined by the implantation 
or/and growth of endometrial tissue postsurgically at the incision site. Most commonly 
accepted theory for scar endometriosis is Direct endometrial implantation to wound edge 
during abdominal or pelvic surgeries. 
The incidence of scar endometriosis has been shown to be less than 2%with the most 
common subtype being post cesarean section. 
Symptoms : Dull aching abdominal pain Dysmenorrhea 
Dyschezia 
Disorders of menstruation Dyspareunia 
Only 20% of women will show up with symptoms 
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Nagaraj and M: A Case Of P2L2 With Scar Endometriosis With Previous Two LSCS
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DIAGNOSIS : 
*USG abdomen shows , irregular walls with low level echos within and occasional high level 
echogenic areas which are blood clots. 
*CT/MRI has no additional advantage than USG Haematological investigations will be 
normal 
However CA-125 is increased in endometriosis although levels are lower than they are in 
ovarian carcinoma 
*Laparoscopic findings : Powder burns / Gunshot lesion 
MANAGEMENT : 
This requires both surgical excision and hormonal suppression 1- Progestational drugs 20-
100mg p/o for 6months, have been used to treat symptomatic 
endometriosis.medroxyprogesterone acetate is mostly used. 
Levonorgestrel containing IUDs has recently been used for treatment of rectovgainal 
endometriosis 
2. Oral contraceptive pills ,can be given cyclic or continuous fashion, however 
monophasic formulation seems more logical than multiphasic pill for continuous therapy.the 
usual regime is continuous treatment with one pill daily for 6-12 months. 
3. GNRH agonist – causes pseudomenopause and pseudo pregnancy.given for 6months. 
4. Gestrinone – is a 19- nortestosterone derivative steroid having androgenic, antiprogestinic, 
antiestrogenic actions,thus extensively used in endometriosis.given 2.5mg-10mg On a twice 
or thrice weekly schedule. 
5. Danazol can also be used. But not used now a days. 
It is believed that hormonal suppression is only partially effective. 
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For endometriosis hormonal suppression may be effective but in scar endometriosis hormonal 
supplements aren’t useful.surgery is the choice. 
Surgical treatment : Excision 
Most effective 
Surgery for the treatment of endometriosis can be performed via laparotomy or laparoscopy. 
Laparoscopy offers advantage over laparotomy in better visualisation,less time,less tissue 
trauma,desiccation,smaller incision and speedy postoperative recovery. Post operative 
adhesions and complications may also be less in laparoscopy. 
Peritoneal implants of endometriosis can be ablated with unipolar or bipolar electro surgical 
instruments or lasers or excised by sharp dissection. 
POST OPERATIVE MANAGEMENT 
In order to control the recurrence, progesterone can be given for 4-5 months. 
If the scar is relatively large then can be given up to 9months. 
ACKNOWLEDGEMENT: None 
 
REFERENCES 
1. Hugh S. Taylor , Lubna Pal , Emre seli. Speroff’s Clinical gynaecology, endocrinology and 
infertility. 9th ed. 2019. 
2. Werner, Moschos , Griffith, Beshay,Rahn, Richardson,Hoffman. Williams 
gynaecology. Study guide.2nd ed. The McGraw-hill companies,2012. 
3. Tanos B, Anteby SO. Caesarean scar endometriosis.Int J Gynaecol 
Obstet.1994;47:163-6 
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Nagaraj and M: A Case Of P2L2 With Scar Endometriosis With Previous Two LSCS
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4. wolf G, Singh K. Cesarean scar endometriosis ;A review , Obstet Gynecol 
surv.1989;44: 
 
 
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A Case Of P2L2 With Scar Endometriosis With Previous Two LSCS

Gunasekaran, Dr. Santosh

Thandaveshwara, Dr.Deepthi

Srinivas, Dr. Keerthana

Digital Journal of Clinical Medicine 
Volume 3 Issue 1 Article 11 
1-1-2021 
A Case Of Neonatal Varicella 
Dr. Santosh Gunasekaran 
JSS AHER 
Dr.Deepthi Thandaveshwara 
JSS AHER 
Dr. Keerthana Srinivas 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Gunasekaran, Dr. Santosh; Thandaveshwara, Dr.Deepthi; and Srinivas, Dr. Keerthana (2021) "A Case Of 
Neonatal Varicella," Digital Journal of Clinical Medicine: Vol. 3: Iss. 1, Article 11. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case Of Neonatal Varicella 
Dr. Santosh Gunasekaran, Dr.Deepthi Thandaveshwara, Dr. Keerthana Srinivas, JSS Medical 
College,JSS AHER,Mysuru  
 
CLINICAL HISTORY: 
A single live term male baby was delivered via emergency  LSCS (i/v/o Antepartum 
Hemorrhage), in a tertiary care center. The maternal obstetric score was G2P1L1 and her 
blood group was O+ve. Antenatal history was uneventful. 
Period of gestation: 40 weeks BW: 2.68 kg. APGAR: 8 & 9 at 1min and  5min respectively . 
No postnatal complications. On day 14 after birth, the baby was brought to the hospital with a 
history of profuse fluid-filled lesions all over the body for 4 days. 
The lesions were first noticed on day 10 of life as small fluid-filled lesions over the forehead 
which gradually spread over the entire body involving palms and soles. No history of fever, 
lethargy,  refusal of feeds, or excessive crying. 
No history of recent Varicella infection or herpes in any family member. 
 
EXAMINATION AND INVESTIGATIONS: 
General examination: 
The baby was active and alert. 
Head Circumference: 32CM 
Length: 48cm 
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Weight: 2.63kg 
Heart rate: 130/min, Afebrile 
Eye examination: 
Mild purulent discharge from both eyes and crusting of lashes noted. Cornea,  conjunctiva, 
and pupillary reflexes were normal. Mild icterus was noted. 
Skin Examination: 
1-2mm clear pleomorphic vesicular lesions from head to toe (including palms and soles) with 
an erythematous surrounding skin. 
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Per Abdomen: 
No organomegaly. 
CNS Examination: 
The tone and activity were normal. 
Neonatal reflexes were present. 
Cardiovascular system: 
S1 S2 heard. No Murmurs. 
Respiratory system: 
Bilateral normal vesicular breath sounds. No added sounds. 
Routine blood investigations such as CBC, RFT, and electrolytes were normal.  
Serum total bilirubin was 13.1 mg/dl. 
Tzanck smear showed acantholytic cells on a  proteinaceous background. 
A skin biopsy performed from the truncal skin  (0.4×0.4cm), showed ballooning 
degeneration of epidermal keratinocytes,  enlarged nuclei, and intranuclear inclusions. 
The dermis was edematous and congested with neutrophil and lymphocyte infiltration. 
Eye swab showed the growth of  Klebsiella 
 
 
 
 
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FINAL DIAGNOSIS: 
Differential Diagnosis: 
1. Neonatal varicella 
2. Neonatal pustular melanosis 
3. Herpes simplex 
Final diagnosis: 
 Neonatal varicella with Ophthalmia neonatorum. 
 
DISCUSSION:  
Varicella in neonates can present in the form of congenital varicella syndrome or neonatal 
varicella. Congenital varicella syndrome develops in <1%  of babies whose mothers are 
infected in the 1st and 2nd trimester, where the offspring will have multiple anomalies. 
3rd trimester poses almost no risk of congenital varicella syndrome, but the child can develop 
herpes zoster in the first or second year of life(1). If the mother gets infected within 3 weeks 
before delivery, then the risk of the baby getting a  disseminated infection is about 20-50%. If 
the maternal infection sets within 5 days before the delivery, the infection chance is high, as 
maternal antibody transfer would not have occurred(2,3). Mortality in those cases would be 
0-3%. However, if such cases exhibit symptoms from day 5 to 12 postpartum,  the mortality 
rate would increase to 20%.  
Transplacental infection can present up to 12 days after delivery, after which the infection is 
likely to be community-acquired(2). In our case, the infection has been noticed 10 days after 
delivery. No similar lesions were found in examining the mother. So it is likely that the 
infection is community-acquired. Recommended diagnostic test is viral DNA amplification 
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by PCR, as it has high sensitivity and specificity. Other reliable tests may include ELISA, 
indirect immunofluorescence, and fluorescence antibody tests.  Virus-specific antibody 
detection is not useful as it may mimic antibodies to  HSV. Moreover, maternal  HSV and 
Coxsackievirus infections may present with a  similar rash. They may serve as a differential 
diagnosis to neonatal varicella (2). 
Neonatal varicella is treated with Acyclovir which was used in this case. Immunoglobulin can 
also be administered (2). A community-acquired infection has a relatively better prognosis 
than maternally transmitted varicella presenting from day 5-12. Prevention of neonatal 
varicella can be achieved by immunoglobulin (VZIG) administration to babies if the mother 
is diagnosed with a varicella rash, 3 weeks before or 7 days after delivery. It can prevent 50% 
of the symptomatic cases and reduce the severity in others(2)(4). The baby and mother need 
not be separated and breastfeeding is not contraindicated (2). 
 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
1. Smith CK, Arvin AM. Varicella in the fetus and newborn. Semin Fetal Neonatal Med. 
2009 Aug;14(4):209–17. 
2. Sauerbrei A, Wutzler P. Neonatal Varicella. J Perinatol. 2001 Dec 1;21(8):545–9. 
3. Sharma CM, Sharma D. A classical case of neonatal varicella. J Clin Neonatol. 2013 
Oct;2(4):200–200. 
4. Blumental S, Lepage PManagement of varicella in neonates and infantsBMJ 
Paediatrics. 
 
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A Case Of Neonatal Varicella

S, Dr. Ruthvik

P, Dr. Shastara

Digital Journal of Clinical Medicine 
Volume 3 Issue 1 Article 9 
1-1-2021 
Acute monoplegia with Incontinence 
Dr. Ruthvik S 
JSS AHER 
Dr. Shastara P 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
S, Dr. Ruthvik and P, Dr. Shastara (2021) "Acute monoplegia with Incontinence," Digital Journal of Clinical 
Medicine: Vol. 3: Iss. 1, Article 9. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
Acute monoplegia with Incontinence 
 Dr. Ruthvik S, 
 Dr. Shastara P, JSS Medical College, JSS AHER,Mysuru  
 
CLINICAL HISTORY: 
A 52-year-old male patient developed insidious onset urinary incontinence 1 month ago. He 
has been on Foley’s catheter for the last 20 days for the same. The patient also complains of 
weakness of the right lower limb for 20 days. The weakness has been progressive and 
involves both the proximal and distal groups of muscles. There is dissociated sensory loss in 
the same limb as well. No history of similar complaints on the left lower limb or both the 
upper limbs. 
The patient now complains of loose stools and burning micturition, associated with increased 
frequency since 3 days. No history of fever, trauma, neck pain or back pain, headache, and 
seizures. No history of neurological illness in the past or in the family. The patient is a known 
case of type 2 diabetes mellitus and hypertension for the last 15 years on medication. He is 
also a known case of diabetic chronic kidney disease on treatment. 
 
EXAMINATION AND INVESTIGATIONS: 
General physical examination – conjunctival pallor present. Bilateral pitting pedal edema 
present. 
Pulse – 84bpm 
BP- 150/90mmHg 
CNS examination – 
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Higher mental functions – Conscious, oriented to time, place, and person. 
Cranial nerves- All cranial nerves are intact. 
Motor system- Tone – spasticity in the right lower limb. 
                         Power- 0/5 in the Right lower limb. 
                         Deep tendon reflexes- brisk in the right lower limb. 
                         Plantar reflex- Extensor on the right side and flexor on the left side. 
Sensory system- Dissociated sensory loss present on the right side, below the level of T4. 
Pain and temperature are lost whereas touch and vibration sensations are preserved. 
No significant motor or sensory changes in the other limbs. 
No cerebellar signs. 
No spinal abnormalities on examination. 
Per abdominal examination– No abdominal distension. No local rise of temperature or 
rigidity was found. The abdomen is non-tender. No organomegaly or mass found. 
CVS examination– S1 S2 heard. No murmurs heard. 
Respiratory system examination– Bilateral air entry present. Bilateral NVBS heard. No 
added sounds were heard. 
 
Complete haemogram revealed: 
-Hb-9.6 gm%, 
-TLC- 7390 cells/mm3. 
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-Peripheral blood smear showed a picture of microcytic hypochromic anemia. 
Urine routine showed 3+ albumin, 18-20 pus cells, and no casts. 
LFT was normal.  
His renal function tests showed blood urea of 83 mg/dl and serum creatinine of 4.0 and 
normal levels of serum electrolytes. 
USG abdomen was done which revealed bilateral grade 1 medical renal disease and 
splenomegaly. 
Urine culture- growth of E. coli. 
MRI of the dorsal spine with whole spine screening revealed the following, 
▪ Syringohydromyelia from C6-T9 with a mild expansion of the cord. 
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 T1 weighted MRI images of the Sagittal view of the spine 
showing syringohydromyelia extending from C6-T9(in white arrows).
 
 
FINAL DIAGNOSIS: 
▪ Acute monoplegia and neurogenic bladder. 
▪ Intramedullary pathology- Syringohydromyelia of the lower cervical and dorsal 
column, from C6-T9. 
▪ Urinary tract infection 
 
DISCUSSION:  
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Syringomyelia is a disorder of abnormal CSF circulation. A syrinx is a fluid-filled cavity that 
anatomically lies within the spinal cord parenchyma or the central canal[1]. Hydromyelia 
refers to a fluid-filled cavity within the spinal cord lined by ependymal, which likely results 
from a developmentally non-obliterated central canal. The two terms are often 
interchanged[2]. 
The natural history of patients is variable and unpredictable. It is interlaced with periods of 
stability and progression. The clinical course progresses over months to years. There is 
an early rapid deterioration that gradually slows down[3]. 
Epidemiological data on syringomyelia is limited. Some studies have found the prevalence of 
syringomyelia to be from 8.4/100,000 to 0.9/10,000 with an ethnic and geographic 
variation[4]. The majority of the patients present between ages 20 to 50 with a mean age of 
30. 
Etiology can be idiopathic, malformations like Chiari-I, post TB sequelae, post-traumatic, 
post-operative meningitis. 
The presentation is highly variable. In most cases, patients complain of pain, muscle 
weakness, temperature insensitivity in the upper limb, spasticity or stiffness in lower limbs, 
progressive scoliosis, bladder incontinence. 
MRI with and without contrast is the investigation of choice. It allows accurate visualization 
of the syrinx in both sagittal and axial planes. MRI easily reveals the location, size, 
and extent of the syrinx cavity. 
All current treatment strategies are directed toward improving CSF flow dynamics. 
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Shunts are indicated for idiopathic syringomyelia. Most commonly used is the 
syringosubarachnoid shunt (SSAS). If this fails syringoperitoneal shunt (SPS) may be used. 
In most cases, shunts are not favored and are used as a last resort because of 
high complication and failure rates. 
Spinal intramedullary tumors such as hemangioblastoma, ependymoma, gliomas are the 
differential diagnoses. Most of these intramedullary tumors will enhance on contrast MRI (a 
syrinx does not enhance on contrast MRI)[5]. 
Prognosis depends on the etiology, the degree of neurological deficit, and the site and size of 
the syrinx cavity. Syrinx diameter of more than 5 mm and associated edema predict a rapid 
deterioration. However, early surgery minimizes deficits and has better outcomes[6]. 
 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
1.Greitz D. Unraveling the riddle of syringomyelia. Neurosurg Rev. 2006 Oct;29(4):251-63; 
discussion 264. 
2. Milhorat T H.Classification of syringomyelia Neurosurg Focus 2000 Mar; 8(3):E1 
3. Bogdanov EI, Mendelevich EG. Syrinx size and duration of symptoms predict the pace of 
progressive myelopathy: retrospective analysis of 103 unoperated cases with craniocervical 
junction malformations and syringomyelia. Clin Neurol Neurosurg. 2002 May;104(2):90-7 
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4.  Weier K, Naegelin Y, Thoeni A, Hirsch JG, Kappos L, Steinbrich W, Radue EW, Gass A. 
Non-communicating syringomyelia: a feature of spinal cord involvement in multiple 
sclerosis. Brain. 2008 Jul;131(Pt 7):1776-82. 
5. Fujii K, Natori Y, Nakagaki H, Fukui M. Management of syringomyelia associated with 
Chiari malformation: comparative study of syrinx size and symptoms by magnetic resonance 
imaging. Surg Neurol. 1991 Oct;36(4):281-5 
6.Logue V, Edwards MR. Syringomyelia and its surgical treatment–an analysis of 75 
patients. J Neurol Neurosurg Psychiatry. 1981 Apr;44(4):273-84 
 
 
7
S and P: Acute monoplegia with Incontinence
Published by Research Connect, 2021


Acute monoplegia with Incontinence

K.S, Dr. Shreeraksha

P, Dr. Shasthara

Digital Journal of Clinical Medicine 
Volume 3 Issue 2 Article 10 
1-1-2021 
Interesting Case of Headache with “Can’t Mix Food & Can’t 
Swallow” 
Dr. Shreeraksha K.S 
JSS AHER 
Dr. Shasthara P 
JSS AHER 
Follow this and additional works at: https://rescon.jssuni.edu.in/djcm 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
K.S, Dr. Shreeraksha and P, Dr. Shasthara (2021) "Interesting Case of Headache with “Can’t Mix Food & 
Can’t Swallow”," Digital Journal of Clinical Medicine: Vol. 3: Iss. 2, Article 10. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
Interesting Case of Headache with “Can’t Mix Food & Can’t Swallow” 
 Dr. Shreeraksha K.S, Dr. Shasthara P, JSS Medical College, JSS AHER, Mysuru,  
 
CLINICAL HISTORY  
A 63-year-old male patient, hailing from Mandya district, a farmer by occupation who is a 
known case of interstitial nephritis, improved AKI and seizure disorder on Tab EPTOIN 
100mg 1-0-2 presented with headache since 10 days, on the right side, moderate to severe in 
grade. 5 days following the headache, he developed slurring of speech and difficulty in 
consuming food. He faced difficulty in consuming food as he could not mix his food with the 
tongue. 2 days later, he developed hoarseness in his voice.  
He had no history of fever, nausea, vomiting, or blurring of vision.  
He had no history of loss of smell sensation, no visual disturbance, no loss of sensation on the 
face, no facial asymmetry, no hearing difficulty or giddiness, no difficulty in neck 
movements. 
He had no history of weakness in any limbs, no muscle incoordination, no loss of 
consciousness, or alteration in behavior. 
EXAMINATION AND INVESTIGATIONS 
An old aged man, moderately built and nourished, well oriented to time, place and person is 
conscious, cooperative, and alert. 
Vitals:  
PR- 80 bpm  
BP- 130/70mm Hg 
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K.S and P: Interesting Case of Headache with “Can’t Mix Food & Can’t Swallow
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RR- 18cpm 
Afebrile 
No pallor/icterus/cyanosis/clubbing / pedal edema/ lymphadenopathy. 
Cranial Nervous System: 
Higher Mental Functions: conscious and oriented 
Normal appearance, well dressed. 
Cranial nerves: 
▪ Glossopharyngeal and Vagus nerve: hoarseness of voice +, uvula deviated to left, gag reflex 
absent on right side, taste sensations lost on posterior 2/3rd of the tongue. 
▪ Hypoglossal nerve: tongue deviated to the right. 
▪ Other cranial nerves are intact.  
Motor system: normal bulk, tone, power 5/5 in all 4 limbs;  
Deep tendon reflexes 2+ in all 4 limbs 
The sensory system: B/L sensations intact on all dermatomes 
 Autonomic system – normal 
Cerebellar signs absent 
Meningeal signs absent 
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Deviation of uvula to left 
Hb- 7.8mg/dl 
Total Leucocyte Count – 6800 Cells/cumm 
Serum Urea – 36mg/dl 
Serum Creatinine – 2.32 mg/dl 
Random Blood Sugar- 118mg/dl 
Serum electrolytes-:  
Sodium -135meq/L; Potassium- 4.4meq/L; Chloride-95 meq/L 
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K.S and P: Interesting Case of Headache with “Can’t Mix Food & Can’t Swallow
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USG ABD & PELVIS: Bilateral small kidneys with mild renal disease. 
MULTIPLANNER MR Venography OF BRAIN – Cerebral venous thrombosis of Right 
Transverse sinus, Sigmoid sinus, and Internal Jugular Vein 
MRV showing thrombosis of 
right transverse sinus, sigmoid sinus, IJV 
DIAGNOSIS 
Bulbar palsy (involving IX, X, XII cranial nerve) secondary to Cerebral Venous Thrombosis 
of Right Transverse, Sigmoid sinus, and Internal Jugular Vein. 
DISCUSSION 
The differential diagnosis for Lower Cranial Nerve palsy: [3] 
They can be classified as: 
1. Nuclear: parenchymal lesions, stroke, hemorrhage, trauma, demyelination 
2. Intranuclear: fascicular, cisternal, canalicular, extra canalicular 
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Causes concerning site: 
-within brainstem: infarction, syringobulbia, motor neuron disease 
– around skull: nasopharyngeal carcinoma, glomus tumor, neurofibroma, jugular venous 
thrombosis, meningitis 
– neck and nasopharynx: nasopharyngeal carcinoma, metastases, trauma, carotid artery 
dissection. 
BULBAR PALSY is the lower motor neuron weakness of muscles whose cranial nerve 
nuclei lie in the medulla (bulb).  [3] 
Cranial nerve palsies are related only in 12% of cases with CVT, most commonly involving 
CN II, IV, and VI. Bulbar palsies related to CVT are even lesser in occurrence. [2] 
CVT is a rare condition affecting the 0.6-7/100,000 population. It is defined as superficial or 
deep venous thrombosis in the brain. [1] 
Thrombosis of the cerebral veins is much less common than arterial thrombosis. Superior 
sagittal sinus is most commonly involved. Thrombus may extend to transverse and sigmoid 
sinus. Deep venous system thrombosis (internal cerebral veins, the vein of Galen, or straight 
sinus) is much less common. 
Causes: Local causes like trauma or infection to the sinuses, otitis media, mastoiditis, 
sinusitis, invasion, or compression of sinuses by neoplastic processes; Systemic causes like 
hypercoagulable states, dehydration. 
 
Clinical features: 
– features due to increased ICP like headache, nausea, vomiting, seizures, papilledema 
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K.S and P: Interesting Case of Headache with “Can’t Mix Food & Can’t Swallow
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– focal/motor deficits 
– if spread to jugular foramen, it can involve cranial nerves 9,10,11,12 causing palsy. 
Investigations: 
1. Hematology: complete hemogram, CRP, coagulation studies 
2. CSF examination to rule out meningitis/ SAH 
3. Imaging: CT or MRI to rule out parenchymal lesions, CT or MR Venography: filling defect 
in the affected vessel 
Treatment: Anticoagulants are the mainstay treatment. The patient can be started on heparin, 
followed by warfarin. Mechanical thrombectomy/ intradural thrombolysis in resistant cases. 
Supportive measures like antibiotics, anticonvulsants, anti-edema measures, and analgesics 
are added. 
ACKNOWLEDGEMENTS: None  
REFERENCE  
1. deVeber G, Andrew M, Adams C, Bjornson B, Booth F, Buckley DJ, et al. Cerebral 
sinovenous thrombosis in children. N Engl J Med. 2001;345:417–23.  
2. Straub J, Magistris MR, Delavelle J, Landis T. Facial palsy in cerebral venous thrombosis: 
Transcranial stimulation and pathophysiological considerations. Stroke. 2000;31:1766–9.  
3.Stuart H.Ralston, Ian D.Penman, Mark W. J. Strachan, Richard P.Hobson, Davidson’s 
principles and practice of Medicine, International edition, 23rd edition, Elsevier publication 
2018 
4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5588642/ 
 
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7
K.S and P: Interesting Case of Headache with “Can’t Mix Food & Can’t Swallow
Published by Research Connect, 2021


Interesting Case of Headache with “Can’t Mix Food & Can’t Swallow”

CLINICAL HISTORY:
A 39 year old male patient presented to our institute with one episode of GTCS and post-ictal headache. No other relevant history was present, no similar complaints were present in the past and no comorbidities. On examination, neurological examination was within normal limits. Blood-work up was also within normal limits

Mettu, Bala Seshank Akshit Reddy, Dr

Hiremath, Rudresh, Dr

Raj, Vinay, Dr

JSS Academy of Higher Education and Research 
Research Connect 
Radiology Teaching Files 
2021 
Oligodendroglioma 
Bala Seshank Akshit Reddy Mettu Dr 
Jss medical college 
Rudresh Hiremath Dr 
Jss medical college 
Vinay Raj Dr 
Jss medical college 
Follow this and additional works at: https://rescon.jssuni.edu.in/radiologyteachingfiles 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Mettu, Bala Seshank Akshit Reddy Dr; Hiremath, Rudresh Dr; and Raj, Vinay Dr, "Oligodendroglioma" 
(2021). Radiology Teaching Files. 4. 
https://rescon.jssuni.edu.in/radiologyteachingfiles/4 
This Neuroradiology is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Radiology Teaching Files by an authorized administrator of Research Connect. 
A. CASE TITLE: Oligodendroglioma 
 
B. CLINICAL HISTORY: A 39 year old male patient presented to our institute with 
one episode of GTCS and post-ictal headache. No other relevant history was present, 
no similar complaints were present in the past and no comorbidities. On examination, 
neurological examination was within normal limits. Blood-work up was also within 
normal limits.  
 
C. IMAGING: 
CT BRAIN PLAIN AXIAL, SAGITTAL & CORONAL VIEWS (Fig. 1): 
Relatively well defined irregularly marginated hypodense lesion measuring 14 x 13 
mm noted in the right frontal lobe with plain CT value of 8-12 HU with marginal 
hyperdensities (plain CT value of 45 – 50HU). Adjacent perilesional edema noted 
causing mild effacement of adjacent sulcal spaces. 
 
   
Figure 1 – Axial plain CT Brain 
   
MRI BRAIN AXIAL T1, T2, FLAIR, DWI, ADC, gradient echo T2*, Axial & 
sagittal contrast enhanced T1 and MR spectroscopy (Fig. 2, 3, 4, 5, 6, 7, 8 and 9): 
Well-defined lobulated cortical based mass lesion noted in right frontal lobe 
measuring 44x 47x 45mm (APx TRxCC) extending upto the body of corpus callosum 
on right side. Lesion appears hypointense on T1WI, hyperintense on T2WI with 
1
Mettu et al.: Oligodendroglioma
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central area of ring hypointensity showing blooming on GRE sequence with no 
diffusion restriction. Anterior component of lesion is bubbly and cystic whereas 
medial and posterior component of the lesion is solid in nature. T2-FLAIR mismatch 
noted. Peripheral hyperintense rim is seen on FLAIR sequences. Minimal 
enhancement of the solid component on post contrast images is seen.  
MRS: Shows decreased NAA with raised Choline peak. CHO: NAA – 2.2. There is 
e/o persistent small peak at 2.5ppm- ? Hydroxy-glutarate peak. 
  
Figure 2 – Axial T1         Figure 3 – Axial T2  
  
Figure 4 - DWI                                     Figure 5 – ADC  
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Figure 6 – Axial FLAIR              Figure 7 – Gradient echo T2* 
 
 
 
   
 
          
   
 
 
Figure 8 – Axial contrast 
enhanced T1  
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Mettu et al.: Oligodendroglioma
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Figure 9 – MR spectroscopy 
D. Diagnosis:  Low grade neoplasm – ? Oligodendroglioma. 
 
E. DISCUSSION: 
Epidemiology 
• Based on the CBTRUS statistical report: NPCR and SEER, 2007-2011, in a 
cohort of 95,564 patients of all age groups and in 10,274 children & 
adolescents (0-19 years) oligodendrogliomas represented ~5.9% and 2.5% 
respectively of glial tumors of the CNS1.  
• Oligodendroglioma is graded by WHO into grade II and grade III 2. In grade II 
oligodendroglioma the median age of diagnosis was 41 years with no gender 
predisposition2.   
 
 
Pathogenesis 
• Based on the WHO classification of CNS tumors 5th edition (2021), diagnosis 
of oligodendroglioma requires the status of IDH mutant with 1p/19q co-
deletion.  
 
 
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General features 
• They are well-defined round/ oval intra-axial mass lesions which are in the 
cortex and subcortical white matter3.  
• Most common presentation is seizures. In GTCS most likely location is mesial 
frontal lobe which includes cortex with fibres connected to the genu of corpus 
callosum. In partial seizures, location is in temporal & orbito-frontal lobes 
which spares the cortex and connected to the genu.  
• The typical fried egg appearance of the individual cells is observed in tumor 
cells4.  
 
Imaging 
• CT Findings3: 
o Location: Usually cortical based and peripheral with expansion of the 
gyrus focally and there can be thinning & remodelling of adjacent 
skull. 
o Appearance: 2/3rd – hypodense. 1/3rd - mixed density. 
o Calcification: Majority shows calcification (~70-90%) which can be 
coarse nodular or clumped calcifications. Gyriform calcifications is 
more specific. 
o Degeneration: Cystic in ~20% cases. Gross haemorrhage and 
perilesional oedema are less common, however does not suggest 
malignant degeneration.  
o Enhancement: Nil to moderate with only 50% of tumors showing 
enhancement. Multifocal patchy enhancement is more likely to suggest 
diagnosis.  
• MR Findings3:  
o Appearance: Hypointense to gray matter on T1WI and 
heterogeneously hyperintense on T2/FLAIR.  
o Calcification: Foci of blooming on T2*.   
o Diffusion: No restriction.  
o Enhancement: Many don’t enhance, but ~50% show moderate 
enhancement.    
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Mettu et al.: Oligodendroglioma
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o MRS: Moderate elevation of the Cho: NAA ratio with an additional 
peak of 2-HG (2-hydroxyglutarate) at 2.25ppm. 
o Perfusion MR: When low grade oligodendroglioma is compared to an 
astrocytoma of the same grade, the oligodendroglioma demonstrates 
high rCBV values. High rCBV values is due to the presence of 
“chicken wire” vascularity.   
Histopathological diagnosis : Anaplastic oligoastrocytoma , WHO grade lll. 
 
REFERENCES: 
1. Ostrom QT, Gittleman H, Liao P, Rouse C, Chen Y, Dowling J, Wolinsky Y, 
Kruchko C, Barnholtz-Sloan J (2014) CBTRUS statistical report: primary brain and 
central nervous system tumors diagnosed in the United States in 2007-2011. Neuro 
Oncol 16(Suppl 4):1–63. 
2. Alattar A, Brandel M, Hirshman B, Dong X, Carroll K, Ali M et al. 
Oligodendroglioma resection: a Surveillance, Epidemiology, and End Results (SEER) 
analysis. Journal of Neurosurgery. 2018;128(4):1076-1083. 
3. Osborn AG, Hedlund GL, Salzman KL. Osborn's brain: imaging, pathology, and 
anatomy 2nd edition. Philadelphia, PA: Elsevier; 2018.   
4. Wesseling P, van den Bent M, Perry A. Oligodendroglioma: pathology, molecular 
mechanisms and markers. Acta Neuropathologica. 2015;129(6):809-827. 
 
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Radiology Teaching Files, Art. 4 [2021]
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Oligodendroglioma

Janardhan, Dr. Anu

Digital Journal of Clinical Medicine 
Volume 3 Issue 2 Article 11 
1-1-2021 
Attention Deficit Hyperactivity Disorder 
Dr. Anu Janardhan 
JSS AHER 
Dr. Kishor M 
JSS AHER 
Follow this and additional works at: https://rescon.jssuni.edu.in/djcm 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Janardhan, Dr. Anu and M, Dr. Kishor (2021) "Attention Deficit Hyperactivity Disorder," Digital Journal of 
Clinical Medicine: Vol. 3: Iss. 2, Article 11. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
Attention Deficit Hyperactivity Disorder 
 Dr. Anu Janardhan Dr. Kishor. M, JSS Medical College, JSS AHER, Mysuru  
 
CLINICAL HISTORY 
A 6-year-old boy, resident of an urban area, studying in 1st standard, from a nuclear family, 
with an elder sister, belonging to lower socioeconomic status presented to the psychiatry 
OPD with his  
mother, with difficulty to sit at one place, difficulty to focus, and increased irritability since 1 
year. The mother reported that the teachers complained of the boy who could not wait for his 
turn in school and was constantly switching between tasks. Teachers also complained about 
his distractibility, as he would do different tasks before completing the one at hand. He has 
often forgotten his belongings at school. He grabs anything in his vicinity and tends to 
destroy those items not realizing the consequences. He has been increasingly demanding and 
throws tantrums if his demands are not met immediately. He has also had physical 
altercations with other children of his age group and even a few who are older than him. 
The child was born by a full-term cesarean section. He was admitted to neonatal care a few 
days post-birth due to respiratory difficulties, and difficulty in feeding. But, there was a delay 
in milestones reported – the mother reports that the child started walking at the age of 2 years. 
Pediatrician evaluation found no abnormality except obesity. 
Negative History: 
No history of any nail biting, thumb sucking, bed wetting, head banging or any self harm. 
EXAMINATION AND INVESTIGATION  
1
Janardhan and M: Attention Deficit Hyperactivity Disorder
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General physical examination: The boy was well built, adequately nourished, conscious, 
oriented to time, place, and person. Not easily cooperative. 
Vitals: Within Normal Limits 
Height: 127cm     
Weight: 35kg 
BMI: 21.7kg/sq.m 
Systemic examination: 
CNS- normal motor and sensory system, reflexes elicited normally 
CVS- Normal S1 S2 heart sounds heard. No murmurs heard. 
RS- Bilateral normal vesicular breath sounds heard 
GI- Soft, non tender abdomen. No organomegaly. Normal Bowel sounds heard. 
Diagnostic Test of Attention Deficit Hyperactivity Disorder(DT-ADHD) was done and the 
scoring suggested a severe deficit in attention, severe hyperactivity, and severe impulsivity, 
and the overall scoring suggested Attention Deficit Hyperactivity Disorder. 
DIAGNOSIS 
Attention Deficit Hyperactivity Disorder (ADHD) 
WHO ICD10 Criteria: 
F90.2, Attention-deficit hyperactivity disorder, combined type 
For a clinical diagnosis of ADHD, an individual must exhibit six or more symptoms of one of 
the types of ADHD and also meet each of the following three criteria: 
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The symptoms caused problems before the age of 7. 
The behavior is abnormal for a non-ADHD child of the same age. 
The symptoms have lasted longer than six months, and they impair school, work, home life, 
or relationships in more than one setting. 
Differential diagnosis: 
Hyperkinesia 
Hyperkinetic syndrome 
Conduct disorders 
Simple disturbances of activity and attention 
DISCUSSION: 
Attention Deficit Hyperactivity Disorder is a disorder of childhood that mainly affects the 
attention, concentration, impulsivity, and activity of the affected children. It affects less than 
5% of children but some studies range 8-20% of children in India, mainly in the primary 
school-going age group(1). If untreated, ADHD affects various domains of an individual’s 
life such as academic difficulties, quality of life,  difficulties in the social domains like 
negative peer status, family functioning (relationship with parents/spouse), unintentional 
injury, and even substance use disorders (2). The most common treatment modalities include 
pharmacological agents, mainly stimulants methylphenidate and modafinil. Non-
pharmacological interventions like intensive behavioral modification treatments are found to 
benefit ADHD in childhood. Other psychotherapies which are beneficial in all age groups of 
ADHD affected are attention enhancing tasks, cognitive-behavioral treatment (3). 
ACKNOWLEDGEMENT: None  
3
Janardhan and M: Attention Deficit Hyperactivity Disorder
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REFERENCES: 
1. Manjunath R, Kishor M, Kulkarni P, Shrinivasa BM, Sathyamurthy S. Magnitude of 
attention deficit hyper kinetic disorder among school children of Mysore city. International 
Neuropsychiatric Disease Journal. 2016:1-7. DOI:10.9734/INDJ/2016/21954 
2. Barkley RA. Global issues related to the impact of untreated attention-deficit/hyperactivity 
disorder from childhood to young adulthood. Postgraduate Medicine. 2008 Jan 1;120(3):48-
59. DOI:10.3810/pgm.2008.09.1907 
 
3. Caye A, Swanson JM, Coghill D, Rohde LA. Treatment strategies for ADHD: an 
evidence-based guide to select optimal treatment. Molecular Psychiatry, 390–408(2019) 
 
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