Monday, 21 October 2019

Glioblastoma or Glioblastoma Multiforme (GBM)

Glioblastoma is most malignant and most frequent primary brain tumor. Glioblastoma Multiforme ( GBM) is also called WHO grade IV astrocytoma and it is the most malignant of the astrocytomas.
Incidence
 It accounts for 12-15% of all intracranial neoplasms and 60-75% of all astrocytic tumors.
Age 
It may manifest at any age, but preferentially affects adults, with a peak incidence at between 45 and 75 years of age. About 1% of patients are younger than 20 years old. primary GBM is more common in older adults between 60-75 years.
Secondary GBMs which constitute about 5% of all GBMs , usually occur about a decade or two decade earlier.
 Location
Cerebral hemispheres are the most common site in adults. Glioblastoma occurs most often in the subcortical white matter and deep periventricular white matter of the cerebral hemispheres. Most affectected sites are temporal, parietal frontal and occipital lobes. Combined fronto-temporal location is particularly typical.
Tumor infiltration often extends into the adjacent cortex and through the corpus callosum into the contralateral cerebral hemisphere. Glioblastoma is notorious for its rapid invasion of neighbouring brain structures. A very common feature is extension of the tumor through the corpus callosum into the contralateral hemisphere, creating the image of a bilateral, symmentrical lesion ( Butterfly glioma).
Glioblastoma of the basal ganglia and thalamus is not uncommon, especially in children. Glioblastoma of the brain stem( malignant brain stem glioma)is infrequent and often affects children.
20% of GBM are multifocal and of which 2-5% are synchronous.
Types of Glioblastoma and clinical features
Two forms of GBM are currently recognized: Primary ("de novo") GBM and secondary glioblastoma. Primary glioblastoma constitute majority, about more than 90%, , which arise de novo.
Secondary glioblastoma arise from a previously pre-existing lower grade glioma. While the two types share similar histology, they differ genetically. Neurofibromatosis type 1 ( NF1), Li Fraumeni and Turcot syndrome demonstrate an enhanced propensity to develop GBM.
The clinical history of the disease is usually short ( less than 3 months in more than 50% of cases). Unless the neoplasm has developed from a lower grade astrocytoma ( secondary glioblastoma).
Symptoms and signs of raised intracranial pressure ( headache, vomiting, papilledema) are common. Seizures , focal neurological deficits  are common. Sometimes patients may present with sudden stroke like features due to acute intratumoral hemorrhage ( in about 2% patients).
Histopathology
Glioblastoma on gross appearance look like Reddish-gray " rind of tumor, with necrotic core with marked peritumoral edema. It shows increased vascularity, and intra-tumoral hemorrhage.
The histopathological features include nuclear atypia, cellular pleomorphism, mitotic activity, vascular thrombosis, microvascular proliferation, and necrosis.
As the term glioblastoma " multiforme " suggests , the histopathology is extremely variable.  The varied tumor cells include: pleomorphic fibrillary astrocytes, gemistocytes, bipolar bland appearing but mitotically active small cells ( including " microglia")and large bizzare multinucleated giant cells. While some lesions show a high degree of cellular and nuclear polymorphism with numerous multinucleated giant cells, others are highly cellular, but rather monotonous.
GBMs generally have a high proliferation index (MIB-1), usually exceeding 10%.
Immunohistochemistry shows GFAP and olig 2 positivity. IDH-1 is very helpful in distingushing secondary GBM (positive) from primary GBM ( negative).
Radiology of Glioblastoma
At least 90 -95% of GBM demonstrate a thick, irregular, enhancing "rind" of tumor surrounding a necrotic core.
CT scan of brain: Most GBMs demonstrate a hypodense central mass surrounded by an iso-to moderately hyperdense rim on non-enhanced CT scan. Hemorrhage is common but calcification are rare. marked mass effect and significant hypodense peritumoral edema are typical ancillary findings.
Contrast Enhanced Computerized Tomography (CECT) of Brain reveals strong but heterogenous irregular rim enhancement. In highly vascular GBMs prominant vessels are seen as linear enhancing foci adjacent to the mass.
MRI of Brain: T1W1 image shows poorly marginated mass with mixed signal intensity . Subacute hemorrhage is common. T2/FLAIR image shows heterogenous intensity with extensive vasogenic edema. Necrosis, cysts, hemorrhage at various stages of evolution are seen. Fluid-debris level is seen in some cases.
Contrast Enhanced magnetic Resonance Imaging ( CE MRI) of brain shows strong but irregular contrast enhancement with central non-enhancing core.
DWI MR : most GBMs do not restrict on diffusion weighted imaging.
DTI may show increased fractional anisotropy and disrupted white matter tracts from tumor invasion.
MR spectroscopy (MRS) may show elevated choline peak and decreased NAA.
On imaging the differential diagnosis of GBM is usually Metastasis and Abscess. Metastasis is usually multiple and occur at gray-white matter junction and non-infiltrating. Intracranial abscess is usually thinner with more regular rim which usually restrict on DWI.



Treatment of Glioblastoma
Neurosurgery and Radiation Oncology intervention: Craniotomy and tumor decpmpression. The cytoreductive surgery followed by chemo and radiotherapy.

Sources:
1. WHO classification of Tumours of the central nervous system Edited by David N.Louis, Hiroko Ohgaki, Otmar D. Wiestler , Webster K.Cavene
2. Handbook of Neurosurgery by Mark S. Greenberg


Tuesday, 12 February 2019

Decompressive Craniectomy(DC), Decompressive Hemicraniectomy, Cranioplasty and Duraplasty

Decompressive craniectomy and decompressive hemicraniectomy are the similar termnologies which are used interchangeably to describe a wide frontotemporoparietal craniotomy on one side of the cranium to reduce the intranial pressure.
This procedure is commonly done in cases of traumatic brain injury and middle cerebral artery ( MCA) infarcts. About 10-15% patients with MCA infarct suffer from progressive clinical detrioration due to increased brain swelling, raised intracranial pressure (ICP) and subsequent herniation. Such space cupying infarct is commonly referred to as malignant MCA infarct. Edema associated with these infarcts is usually observed between the second and fifth day after the index event. Malignant MCA infarct is associated with poor prognosis.Its fatality rate is about 80% and most survivors are left with severe diability. Medical management of malignant MCA infarction is generally ineffective and requires a surgical intervention in the form of decompressive craniectomy for its relief. Surgical decompression reduces the risk of death or disability. An observation study conducted at AIIMS, Delhi had reported that patients who were operated within 48 hours from onset of smptoms and who were less than 60 years old showed better clinical improvement following decompressive craniectomy.
All patients with life threatening malignant MCA infarction indicated to undergo (DH) on the basis of clinical assessment basedon National Institute of Health Stroke Scale [ NIHSS], Glasgow oma scale (GCS) and neuroimaging.

Criteria for Surgery in cases of malignant MCA infarct are:
                        *NIHSS score more than 16
                         * GCS score less than 13
                         * Decrease in level of consciousness
                          * Clinical signs of herniation
                          *Presence of radiological evidence

A large Fronto temoporo pariental free bone craniotomy of about 12 centimeter to 15 centimeter is elevated with lax duraplasty. The free bone is placed in the subcutaneous fat pocket in the right iliac region of lower abdomen inferolateral to the umbilicus. When patient improves the cranioplasty is done with the same preserved bone.
DH in large MCA stroke patients leads to markedly improved survival and better functional outcome ( motor and language) and recovery in motor and ahasia recovery is progressive and sustained after 1 year.[1]
Decompressive craniectomy was originally decribed by Cushing. It is used in cases of refractomy intracranial hypertension where convenional therapies have failed. The technique involves removal of a large bone flap and opening the dura. The dura may be left open as it is or a graft may be used to enlarge the volume of the dural compartment. Once the period of intracranial hyertension has settled and patinet has improved, cranioplasty is done with the preserved free boen cranial flap. Study conducted at AIIMS by Sinha et al has reported that DC can ameliorate the secondary damage due raied ICP in cases of traumatic brain injury (TBI).

References
1. Long term outcome of decompressive hemicraniectomyin patients with malignat MCA infarcts: A prospective observational study. VK Rai et al , AIIMS, Delhi in Neurology India, 2014
2. Decompressive craniectomy in traumatic brain injury : a single center, multivariate analysis of 1,236 patients at a tertiary care hospital in India. Sumit Sinha et al, Neurology India
3. Ramamurthy and Tandons' Manual of Neurosurgery


Non-contrast CT scan of head of the patient after 6 months of Middle cerebral infarction showing a large area of the infarct with large craniectomy defect. Now patients' CT scan does not suggest any midline shift so patient may undergo cranioplasty.

Craniotomy bone flap is preseved in the subcutaneous fat in the right iliac fossa region in abdomen.






           

Sunday, 20 January 2019

ANTIBIOTICS

Antibiotics are the medicines which are used to treat infections. Infections may be due to bacteria, fungi or virsuses. Almost everyone suffers from infection someimes in his life time.

Being infected is a bad feeling and everybody dislikes it. Sometimes, these infections are so dreaded that it is better to get immunity against such bad infections. So, vaccines are used to present such bad infections, Commonly used vaccines are BCG ( to prevent Tuberculosis), DPT ( to prevent Diphtheria, Pertusis and Tetanus), Anti Hepatitis B Surface antigen Vaccine ( to prevent infection against hepatitis B), Polio vaccine, etc.

But, all infections are not so dangerous, like common cold, sore throat, and small furuncle or small reddish pimple. Such infections usually subside by themselves due to the immunity of our own body. This immunity is mainly provided by white blood cells (WBCs) and lymphocytes present in our body. These act like Policemen patrolling our internal security. These security personnel detect and kill the foreign microbials or microorgaisms like bacteria.

Sometimes, infecions may overwhelming and required to be treated with antibiotics. Like common cold not subsiding and persisting for longer duration with superadded bacterial infection or sinusitis. Or, sore throat associated with yellowish sputum with cough and fever. So, we need to take antibiotics to treat such infections.

Infections may be superficial or deep, local or systemic. The infection depends upon virulence or the microorganism, resistance of the person, and living conditions. Like persons with diabetes with uncontrolled blood sugar level and patients on long term steroids have low resistance or immunity against the infecive microrgansms. Person living in crowded places with other people infected with communicable diseases are prone to acquire infections of the airborne diseases like tuberculosis, influenza, etc.

Skin infections are commonly caused by Staphylococcus aureus and Streptococcus. Invention  of Penicillins in 1928 by Scottish researcher, Alexander Flemming, made a great difference to the outcome of patients with infecions.

Sir Alexander Fleming

Sir Alexander Fleming was a Scottish physician, microbiologist, and pharmacologist. His best-known discoveries are the enzyme lysozyme in 1923 and the world's first antibiotic substance benzylpenicillin from the mould Penicillium notatum in 1928. The simple discovery and use of the antibiotic agent has saved millions of lives, and earned Fleming – together with Howard Florey and Ernst Chain, who devised methods for the large-scale isolation and production of penicillin – the 1945 Nobel Prize in Physiology/Medicine.


Penicillin was effective against fatal infections caused by bacteria. But, over time, these bacteria outsmarted the drug and developed resistance to these drugs. But, consistent efforts by the physicians, microbiologists, pharmacologists, biotechnologists and other inventors led to the development of many anti-microbial drugs which are commonly known as antibiotics.

So, commonly uses antibiotics are penicillins, cephalosporins, tetracyclines, macrolides, quinolones, anti-viral drugs, anti-fungal drugs, etc.
Common bacteria are described as Gram positive or Gram- negative. Gram positive bacteria are stained positively by Gram stain. 
Some bacteria produce exotoxins and some produce endotoxins. 
Tbe bacteria which produce exotoxins are Cornyebacterium diphtheriae, Clostridium tetani, C.botulinum, C.perfringens, Bacillus anthracis, Staphylococcus aureus, Streptococcus pogens ( all are examples of Gram positive bacteria).
Gram negative bugs which produce exotoxins are E.coli, Vibrio cholerae, and Bordetella pertusis. 
Endotoxin is a polysaccharide and is found in the cell wall of Gram-negative bacteria. 
Some bacteria do not stain well with Gram-stain, like Treponema, Rickettsia, Mycoplasma, Legionella pneuophila, Mycobacteria and Chlamydia.
For treponemes-darkfield microscopy and fluorescent antibody staining is used. 
Mycobacteria are acid-fast bacilli. Legionella is stained with silver stain.

Gram positive bacteria are broadly classified in 2 groups; Cocci and Bacilli.
Gram positive cocci are classified into two; catalase positive clusters ( Staphylococcus) and catalase negative chains ( Streptococcus). 
Catalase postive staphylococci are further classified into two groups as Coagulase positive ( S.aureus) and coagulase negative [ Staphylococcus epidermidis ( Novobiocin sensitive) and Staphylococcus saprophyticus ( Novobiocin resistant ].
Gram postive and catalase negative chains of cocci are Strptococcus. On the basis of hemolysis Streptococci are divided into 3 categories: Green ( partial ) hemolysis; Sterptococcus pneumoniae, Clear hemolysis Streptococcus pyogens ( group A Bacitracin sensitive), S.agalactiae ( group B, Bacitracin resistant) and 3rd category of streptococci with no hemolysis examples are Enterococcus ( E.fecalis) and Peptostreptococcus( anaerobe).




Exapmple of Gram positive bacilli ( rods) are: Clostridium ( anaerobe), Cornyebacterium, Listeria and Bacillus.


Gram negative bacteria which appear pink are broadly classified into three groups : Cocci, C0ccoid rods and rods. 
Gram negative cocci are Neisseria mningitidis and N.gonorrhoeae. These two are differentiated on the basis of Maltose fermenter chacteristic. N. menigitidis is Malose fermenter and N. gonorrhoeae is Maltose noferenter.

The examples of cgram negative coccoid rods are Hemophlus influenzae, Pasteurella, Brucella and Bordetella pertusis.

Gram negative rods are further subdivided into two subtypes based Lactose fermenter characteristic. Lactose fermenter gram negative rods are Klebsiella, E,coli and Enterobacter which are Fast fermenter and Citrobacter, and Serratia Slow fermenters.
Lactose nonfermenter gram negative rods are subdivided into two groups, based on oxidase property. Oxidase positive are Pseudomonas and oxidase negative are Shigella, Salmonella and Proteus.






Penicillin C is for intravenous use and Penicillin V is for oral use. 
Penicillin binds penicillin-binding proreins , blocks transpeptidase cross-linking of cell wall and activates autolytic enzymes. It is bactericidal for gram positive cocci and rods, gram negative cocci and spirochetes.

Methicillin, nafcillin have narrow spectrum and used against penicillase resistant Staphyloccus aureus.

Ampicillin, Amoxicillin have wider spectrum, penicillanse sensitive, also combined with clavulanic acid ( penicillanase inhibitor) to enhance spectrum. Amoxicillin has greater oral bioavailability than ampicillin. These two extended-spectrum penicillin and are useful against certain gram positive bacteria and gram negative rods ( Hemophilus influenzae, E.coli, Listeria monocytogens, Proteus mirabilis, Salmonella and enterococci). 

Carbenicillin, Piperacillin and Ticarcillin are extended spectrum penicillin and useful against Pseudomonas  and gram negative rods , susceptible to penicillanase, used with clavulanic acid.

Cephalosporins are beta lactam drugs. It inhibits cell wall synthesis 


Imipenem
      Imipenem is a broad spectrum, beta lactamase-resistant carbapenem. It is always administered with cilastatin which is inhibitor of renal dihydropeptidase 1 to decrease inactivation in renal tubules. Ii is used against gram positive cocci, gram negative rods and anaerobes. It is drug of hoice against Enterobacter. Its toxicity includes GI distress, skin rash, and CNS oxicity ( seizures).

Vancomycin

Aminoglycosides

Tetracyclines 

Macrolides

Chloramphenicol

Clindamycin

Sulfonamides

Trimethoprim

Fluroquinolones

Metronidazole




References: 
Wikpedia

Alexander Fleming (1881–1955): Discoverer of penicillin, Siang Yong Tan, Yvonne Tatsumura

Singapore Med J. 2015 Jul; 56(7): 366–367. doi: 10.11622/smedj.2015105















Wednesday, 14 November 2018

Intramedullary spinal cord Tumors

Intramedullary tumors are the tumors which are present in the spinal cord, i.e., inside the pial covering and substance of the spinal cord itself.



This diagram explains the location of the intramedullay tumors. Piamater is the innermost of three meninges ( Duramater, Arachnoid and Piamater). It covers the spinal cord. So the tumors outside of it may be IDEM ( intradural extramedullary) or extradural lesions. 

Spinal tumors are are classified as

 (1) extradural,

(2) intradural extramedullary, and

 (3) intradural intramedullary.

Extradural tumors are the most common spinal tumors and are usually of metastatic origin. 

Intradural Extramedullary (IDEM) tumors are mainly neurofibroma and meningioma.

Intradural intramedullary lesions comprise 20 to 30% of all primary spinal cord tumors.

Gliomas make up 80% of all intramedullary tumors. The gliomas are further subdivided into astrocytomas (60 to 70%) and ependymomas (30 to 40%). Hemangioblastomas are the third most frequent intramedullary spinal cord (IMSC) tumors, comprising 2 to 15% of all intramedullary tumors. Metastatic intramedullary tumors are rare but present in 2% of all intramedullary tumors. Lipomas are commonly associated with spinal dysraphism.
Intramedullary tumors constitute about 35-40% of all intraspinal tumors in children. In children intramedullary tumors are mainly developmental in origin, like dermoid, lipoma and epidermoid). In adults intramedullary tumors may arise later in life, like astrocytoma, ependymoma and hemangioblastoma.

Gliomatous and nongliomatous tumors constitute 90 and 10% respectively.

In 75% cases, the astrocytmas extend over 4 or less 4 vertebral segments. In some cases the lesions extends throughout the spinal cord, for example holocord astrocytomas.

Half of the central nervous system ependymomas are located in the spinal cord and, of these, 50% are located in the filum terminale. The next common site is the cervical cord.

Glioblastomas are not common.

Hemangioblastoms are rare, consist of less than 2% of primary spinal cord tumors.

Clinical presentation depends upon the site and size of the lesion.

MRI of spine with contrast is the investigation of choice.




                                  Intraoperative image of my adult patient where tumor is seen after posterior midline myelotomy. Histopathology of the tumor was suggestive of Pilocytic astrocytoma ( WHO grade 1 tumor)

The operating microscope, bipolar coagulators, intraoperative physiological monitoring ( somatosensory evoked potenial monitoring, motor evoked potential ) , microscissors, microdissectors, small tumor holding forceps, Cavitron Ultrasonic Surgical Aspirators (CUSA) , intraoperative USG ( Ultrasonography) are good for safe excision of intramedullary lesions.


References

Samartzis D, Gillis CC, Shih P, O'Toole JE, Fessler RG. Intramedullary Spinal Cord Tumors: Part I-Epidemiology, Pathophysiology, and Diagnosis. Global Spine J. 2015;5(5):425-35. And references as numbered below

Mechtler L L, Nandigam K. Spinal cord tumors: new views and future directions. Neurol Clin. 2013;31(1):241–268.

Grimm S, Chamberlain M C. Adult primary spinal cord tumors. Expert Rev Neurother. 2009;9(10):1487–1495.

DeSousa A L, Kalsbeck J E, Mealey J Jr, Campbell R L, Hockey A. Intraspinal tumors in children. A review of 81 cases. J Neurosurg. 1979;51(4):437–445.

Mandigo C E, Ogden A T, Angevine P D, McCormick P C. Operative management of spinal hemangioblastoma. Neurosurgery. 2009;65(6):1166–1177.

Ravi Ramamurthy. Spinal Intramedullary Tumours. Chapter 130, Volume 2, in Textbook of Operative Neurosurgery, B.I Publications Tvt Ltd, New Delhi, Pages1107-1113.




Tuesday, 12 June 2018

Surgical cases of Tuberculosis of Central Nervous System


Tubercuolosis (TB) continues to be a major public health concern, especially in developing countries. TB is one of the top 10 causes of death worldwide . In 2016, 10.4 million people fell ill with TB; and 1.7 million died from the disease. In 2016, an estimated 1 million children became ill with TB and 250,000 children died of TB. 
Tuberculosis of central nervous system (CNS) can be treated effectively with anti-tubercular therapy (ATT). ATT duration for treatment of CNS TB is 12 months ( 2 months intensive phase and 10 months continuation phase). Some cases of CNS TB require neurosurgical intervention. I am presenting 3 cases of cranial TB where the presentations were unusual leading to delay in the diagnosis. All these three cases were effectively treated with neurosurgery along with ATT.

Patient 1 was a middle aged female with history of headace of long duration. CT scan of head revealed extradural collection beneath the frontal bone. The frontal bone was thickened. This was unusual as duration of symptom was in years and the bone above the lesion was thickened.
 Surgical image showing  pus coming out of frontal bone bur hole

As intensity of the headadche increased , patient was advised surgery. On craniectomy about 60 ml of pus came out under pressure. Patient became asymptomatic after surgery and ATT.

Patient 2 was a middle aged male with history of trauma and swelling over the vertex of skull about 15 days back. Patient was suspected to have scalp hematoma and swelling and was advised antibiotics and analgesics. CT scan showed a scalp swelling over the cranium. Patient underwent surgery and about 40 mL of pus was drained and it was sent for culture/ sensititivity, Gram stain , AFB stain. It came out positive for Staphylococcus. But, despite of prescribing antibiotic according to sensitivity, wound was not healing. Later, wound was re-explored and remaining pus drained out and bony osteomyelitis of the cranium was evident. Craniectomy of the pariental bone at the vertex was done and sent for histopathological examination. Biopsy was suggestive of tuberculosis.


                                                  Surgical image of the patient showing calvarial osteomyelitis

Patient's surgical wound healed with antibiotic and ATT. He became asymtomatic after taking ATT.

Patient 3 was a child of about 14 year age. He presented in emergency of my Institute with history of headache, vomiting, deterioration of conscious level, weakness of right half of body and recurrent seizures. CT scan of the brain and MRI of brain with contrast revealed intracranial subdural hypodense collections in interhemispheric fissure and left fronto-parietal convexity of brain.


                         Surgical image showing burr hole in the frontal bone and pus coming out of subdural space
Frontal region incision was made and single burr hole made in frontal bone under general anesthesisa. Dura was coagulated and incision made in dura. About 80 mL of thick pus came out under pressure. Patient improved after surgery and ATT.

Many types of neurotuberculosis have been described; most common intracranial forms are tuberculous meningitis and tuberculomas.Tuberculous brain abscess and subdural empyema are extremely rare manifestations of central nervous system tuberculosis. Subdural empyema or collection of pus in the subdural space is mostly pyogenic.  Intracranial tubercular subdural empyema is very rare in pediatric population. Various  diagnostic  modalities  and  treatment options  are  available  for  managing central nervous system tuberculosis (CNS  TB).   But, outcome  remains of CNS TB is poor as clinicians  face  many challenges  in  the  management  of  the  tubercular infection  of  the  brain  and  spinal cord.
Treatment of CNS TB is challenging due to lack of specific biochemical tests and inability to get the pathological sample from deeply located eloquent areas of CNS without causing any neurological deficit. Moreover, it is unnecessary to operate for biopsy in a patient who has presented with a very small granulomatious lesion in brain or spinal cord. In such as situations neuro-radiology helps in managing CNS TB and it may be the only source of establishing diagnosis and evaluating treatment response. Role of radiological investigation has expanded from the initial diagnosis to the therapeutic interventions. In some Muli-drug- resistant (MDR) CNS TB cases, stereotaxy or Ultrasonogram (USG) or CT guided biopsy helps in obtaining pathological sample and drug sensitivity testing. A regular clinical and neuro-radiological follow-up is mandatory during the entire course of anti tuberculous therapy to take prompt decisions to change ATT and to reduce morbidity and mortality associated with CNS TB.

Traditionally, culture for the mycobacterium is considered as gold standard for diagnosis of TB. But,  tuberculin  test,  biochemical  investigations and  AFB  stain  and  culture  of  the  cerebrospinal fluid  or  granulation  tissue  provide  little  support for the management of CNS TB or its sequelae.  There should be high index of suspicion for the CNS TB in a patient who is from an endemic region. There may be extensive tubercular involvement of CNS even  in  absence  of  the  history of pulmonary diseases,  tubercular  contact  or  any  other neurological  deficit.  It is difficult  to assess  the therapeutic response in the early follow up period in view of the lack of sensitive and specific tests. Vigilant clinical observation and imaging studies is required in the early follow up period to identify the  worsening  or  new  emerging  signs  in  the patients  of  CNS  TB.  Imaging  studies  are becoming  the  major  decisive  tools  for  the empirical  therapy  and  early  follow  up  of  the patients to evaluate the therapy.
Intracranial tubercular subdural empyema can be effectively treated with ATT and burr hole evacuation of pus. Close clinical observation, neuroradiological assessment with CT scan or MRI and prompt therapeutic interventions   are  necessary  for starting the empirical anti-tuberculous  therapy and early follow up of the patients to evaluate the therapeutic response. 

 In all these cases pus was negative for Acid Fast Bacillus (AFB). This is very common observation. So, high index of suspicion and close follow up is required in suspected cases of cranial TB. Clinical observation with empirical ATT is key in the management of CNS TB cases.

References
1.       An unusual presentation of neurotuberculosis: subdural empyema . Case report. Cayli SR, Onal C, Kocak A, Onmus SH, Tekinen A. J Neurosurg 2001 Jun; 94(6): 988-91
2.       Global tuberculosis report 2017, WHO ( www.who.int)
3.       Pediatric intracranial subdural empyema caused by Mycobacterium tuberculosis- a case report and review of literature. Banerjee AD, Pandey P, Ambekar S, Chandramouli BA. Child Nerv System. 2010, Aug: 26(8): 117-20.doi 10.1007/s00381-010-1157-3 Epub 2010 May 2
4.       Intracranial tuberculous subdural empyema: case report. Van Dellen A, Nadvi  SS, Nathoo N, Ramdial PK. Neurosurgery 1998, Aug; 43(2), 370-3.
5.        Vijaykumar B, Sarin K, Girija Mohan. Tuberculous brain abscess and subdural empyema in an immunocompetent child: Significance of AFB staining in aspirated pus. Ann Indian Acad Neurol. 2012, Apr-Jun, 15(2):130-133.
6.       Gautam VKS, Khurana S & Singh R. Diagnostic and therapeutic challenges in the surgical management of CNS tuberculosis. International Journal of Medicine and Health Sciences, 2013, Vol-2;Issue-2, 161-169. 



Wednesday, 6 June 2018

Concussion

Concussion means transient loss of consciousness due to head injury.
Concussion is also known as Mild Traumatic Brain Injury (MTBI). 
It may be described as alteration of consciousness without structural damage as a result of head trauma. 
It is transient loss of consciousness or alteration in mental status like alteration in conscious level,  disturbance of vision or balance due to head injury.
Trauma to the head may cause sudden linear or rotational movement of the brain.  This sudden acceleration and deacceleration  movements of the brain and brain stem disrupts the normal cellular activities in the brain ( including fornix, corpus callosum, temporal lobe, frontal lobe) and in the the reticular activating system of the midbrain.  

Although, concussion is considered as mild head injury but sometimes it has sequelae. Headache, confusion, amnesia, blurring of vision, dizziness, fatigue  may persist for some time.  More alarming long term sequelae are the cognitive impairment, sleeplessness, difficulty in concentration,  irritability, anger, behavioural abnormalities, or maladjustment in the work or studies.
Plain CT scan of brain is the investigation of choice. It is normal in cases of concussion because it is a physiological impairment and so, no anatomical abnormality is seen on non-contrast CT scan of the brain. MRI of the brain is not required and  is unnecessary. MRI will demonstrate abnormalities in up to 25% of cases where CT is normal. But, I do not suggest MRI in cases of concussion because CT actually guides the treatment. So, if CT is normal there is nothing serious and no active neurosurgical treatment is required. MRI just adds to the apprehension of the patients and their relatives and it does not provide any additional information of any use to the neurosurgeon.

Symptoms usually resolve in approximately two weeks. But, symptoms may persist for longer period.
Every person with post traumatic concussion requires emotional support. 
Patient’s caregivers, family members, teachers and co-workers and colleagues must understand that some symptoms like irritability, headache, dizziness may be sequelae of concussion.  So,  a sympathetic and considerate attitude should be adopted towards the person who had suffered mild head injury with concussion and is experiencing long term sequelae of mild head injury. 
Symptomatic treatment of like dizziness may be trated with Betahistine or Cinnarazine. Headache is a common complaint and requires both medical and psychological support.
Neurotrophic vitamins like vitamin B complex, Methylcobalamin,  vitamin E are useful.  Anxiety, sleeplessness are very well managed with tablet Clonazepam 0.25 mg at night and Psychological support.

Monday, 1 January 2018

Spina Bifida, Spinal Dysraphism, Myelomeningocele and Meningocele

Spinal dysraphism means a spectrum of congenital anomalies of the spine and spinal cord.

Spina bifida is a common form of spinal dysraphism. The term spina bifida includes a wide variety of anomalies.
  
Congenital defect in the spine leads to spina bifida. This can be of two types: spina bifida occulta and spina bifida aperta.

In spina bifida aperta; visible lesion, like a swelling over the midline of the back may be noticed at the time of birth of a child. Such spinal dysraphism is known as Spinal Bifida Aperta.

But, a child may be having some abnormalty of the spine or spinal cord but without any externally visible lesion and overlying skin is intact, then it is known as Spina Bifida Occulta.  This defect of the vertebrae of the spine of a child may not be visible at the time of birth and there may be no visible exposure of meninges or neural tissue. And, there may be congenital defect only in the lamina of the vertebrae of the spine without any involvement of underlying spinal cord. This is known as spine bifida occulta.

But, in spina bifida aperta there is a visible or open defect in the spine. There may be congenital defect in vertebral arches with cystic distension of meninges which is filled with CSF and is known as Meningocele. If, in this congenital defect of the vertebral arches there is a cystic dilatation of meninges and cerebrospinal fluid along with neural tissue or spinal cord ( Myelon) , then it is known as Myelomeningocele. If Myelomengocele contains fat tissue, then it is known as Lipomyelomengocele.

Myelmeningocele is one of the congenital open neral tube defect present at the birth on the back of the newborn.

It is a common type of congental defect of the spine and its incidence is about 1 in 1,000 live births. Better nutrition and folic acid suplementatiion during the antenatal care of the mother decrease its occurrence.

Ultrasound study during the early antenatal care detects any occurrence of myelomeningocele in a fetus during pregnancy.

A newborn child should be assessed for any sensory or motor deficit due to meningocele or myelomeningocele. There may be associated congenital lesions, like cardiac lesions. Myelomeningocele may be associated with congenital hydrocephalus. So, MRI of the spinal cord and brain is investigation for choice for assessing a case of meningcele. MRI may show whether a swelling on the back of a child is only flled with CSF or does it contain any neural tissue. It detects any intraspinal extension, associated intrasinal dermoid, lipoma, dermal sinus, spina bifida, spinal dysrahism like duplication of the cord, any bony spur between the duplicated cord, Chiari malfomation, syrinx, hydrocephalus, thickened filum terminale, etc. So, MRI helps in diagnosis, surgical planning and predicting prognostic outcome.
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