Cervical Pott’s and retropharyngeal abscess

A 50 yo male with compressive myelopathy. Severe neck pain.
MRI Cervical Spine

Sagittal T2 and T1 images show altered marrow signals involving C2 and C3 vertebral bodies with diffuse marrow odema on STIR. Intervening C2-3 disc is destroyed with endplate erosions. An associated prevertebral abscess (green astricks). The adjacent anterior epidural abscess (yellow astricks) causing significant cord compression.

Imagingwise : Cervical vertebral Osteomyelitis with an associated epidural and prevertebral abscess.

Discussion:
Retropharyngeal or pre vertebral abscess in adult is usually develop secondary to direct invasion of pyogenic bacteria after direct trauma to pharynx followed by secondary involvement of adjacent cervical spine.
However there may be a pre exiting cervical osteo myelitis with an associated prevertebral abscess, tuberculosis as a cause is not an unusual in endemic areas like india.

The incidence of tuberculosis is increasing in parallel with the growing numbers of immunocompromised patients.
Presentation is variable either with cord compression due to pathological fracture, an associated epidural abscess or with respiratory distress due to an associated prevertebral abscess. Awareness of this may lead to early diagnosis and treatment.

Tuberculosis or Pott’s disease of spine has predilection for dorsal region followed by lumbar. Cervical region is uncommon.
CV junction contributes ~ 0.3 to 1% of total tubercular spondylitis.

It is important to understand the fact that anti tubercular therapy is the crucial factor in treatment of this condition and not the surgery.  But when neurologic deficits are present due to cord compression, debridement and anterior spinal fusion combined with antituberculous chemotherapy is ideal.

Intracavernous ICA Curvature

3 D TOF Non contrast MR Angiography of brain shows right ICA cavernous portion is medially deviated in sella. Normally cavernous ICAs has para sellar course. 

This sellar course of right ICA is a normal anatomical variation.

In this case left cavernous ICA show normal course and angulations.

When both the ICA show such medial deviation in sella and may touch each other, known as kissing carotids - a rare variant. Mostly noted incidentally during CT or MR Angiography.  Can mimic pituitary disease due to pituitary stalk compression and may complicate trans sphenoidal surgery.

Heterotrophia

A 9 y o boy  with history of seizures. 

Here are his Non contrast CT, MRI Axial FLAIR, T1 and T2w images of Brain. 

There are multiple indentations in the wall of lateral ventricles due to sub ependymal nodules with density same as that of cortical gray matter on CT and signal intensity on MRI.

Imaging diagnosis : Nodular variety of multifocal heterotrophic gray matter. 

HETEROTROPHIA

A congenital disorder of abnormal neuronal migration.
Gray matter stuck at wrong place.

Can be inherited or acquired (from maternal trauma, infection or toxin)

Normally sub ependymal germinal zone proliferates and form neuroblasts and glial cells which then migrates outwards towards cerebral convexity forming an outer cortical grey matter and inner white matter. Any interruption or arrest in the normal course of this neuronal migration leaves heterotrophic neuronal deposits. These being gray matter deposits follow same density and signal intensity as that of cortical gray matter, non enhancing.

Types:
Sub ependymal nodular heterotrophia – a focal or multi focal subependymal nodules.
Band heterotrophia – alternate band of gray and white matter , ‘ double cortex’.

Clinical presentation : 
Seizures is most common, delayed milestones.

DDs:
Closest differential is subependymal nodules of Tuberous sclerosis which often shows an associated calcification. 

Treatment:
Surgery reserved for intractable Sz.
Resect small accessible epileptogenic nodules.
Corpus callosotomy if bilateral or diffuse unresectable lesions.

ICA can be the cause of thyroid swelling

A 15 yo girl with painless long standing mild right side neck swelling in the region of thyroid, swelling is non tender, does not move with protrusion of tongue.

Usg of thyroid show both lobes of thyroid of equal size and normal in echotexture.

MRI Axial sections of neck:

Volume of both the lobes of thyroid is equal, signals are identical and normal.

Asymmetry in their shape of thyroid lobes due to right side ICA immediately posterior to right lobe causing mild anterior displacement of right lobe.

Caliber of right ICA is normal, just the course is abnormal.

Conclusion: ICA being immediately posterior to the otherwise normal thyroid giving rise to thyroid swelling clinically. 

Isolated sagging of frontal lobe

A young female with long standing mild headache.

Axial CT sections show a doubtful overcrowding of structures at supra sellar cistern. Rest of the brain parenchyma show normal attenuation.

Axial T2 images show more convincing obliteration of supra sellar cistern, supra chiasmatic cistern to be specific. Mid brain antero posteriorly elongated and appears to be compressed between temporal lobes.

Sagittal T1 section clearly depicts frontal lobe particularly the anterior commisure portion of corpus callosum sagging down in supra chiasmatic cistern.

Imagingwise to support intra cranial hypotension, there is no marked sagging of brain stem. Pons, Medulla and cerebellar tonsils are at normal level. There is no medialisation of lateral ventricle with compression. No sub dural collection.

Conclusion: isolated sagging of frontal lobe and anterior comissure of corpus callosum in supra chiasmatic cistern. Clinical significance of this finding to patient’s complaint is doubtful. Patient is advised follow up imaging. 

Cerebral Microbleeds

T2* GRE MRI sequence has high sensitivity in detecting cerebral microbleeds, which appear as small punctate (dot-like) hypointense lesions located widespread in bilateral cerebral cortical white matter , basal ganglia , thalami, cerebellum as well as brain stem and are histologically characterized by hemosiderin deposits with tissue damage.

Generally considered to be clinically silent.
Are strongly associated with intracerebral haemorrhage, hypertension, lacunar stroke and ischaemic small vessel disease, and have generated interest as a marker of bleeding-prone microangiopathy.
Also hypothesized that they would cause cognitive dysfunction.  (David J. Werring, Duncan W. Frazer, Lucy J. Coward, Nick A. Losseff,  Hilary Watt, Lisa Cipolotti, Martin M. Brown and H. Rolf Ja¨ger; Cognitive dysfunction in patients with cerebral microbleeds on T2*-weighted gradient-echo MRI; Brain (2004), 127, 2265–2275)

April 22, 2009 — A new analysis from the Rotterdam Scan Study shows that cerebral microbleeds on MRI are more prevalent in elderly subjects who use platelet-aggregation inhibitors than in nonusers.
Their location in the brain is thought to reflect their underlying origin; microbleeds in infratentorial location are thought to relate to hypertensive or arteriosclerotic microangiopathy, while those in the strictly lobar brain sites result from cerebral amyloid angiopathy, a bleeding-prone state, the use of platelet aggregation inhibitors and anticoagulants in these patients has been found to be associated with increased occurrence of symptomatic hemorrhage.

Scoliosis and Syrinx Association

The association of scoliosis with syringomyelia is well established (Woods and Pimenta 1944; McRae and Standen 1966). Baker and Dove (1983) were the first to report scoliosis as the presenting sign of otherwise asymptomatic syringomyelia and this has since been confirmed by others (Raininko 1986; Isu et al 1992; Lewonowski, King and Nelson 1992). Zadeh et al (1995) found ten cases of syringomyelia in 12 patients with idiopathic scoliosis who had been selected for MRI after the identification of asymmetrical or absent superficial abdominal reflexes.

The pathophysiology of the development of scoliosis with syringomyelia has not been yet established.

Some authors have reported stabilization or improvement of scoliosis after syrinx drainage. yet other authors have reported questionable or no effect of drainage on curve progression.

Shrinkage of syringomyelia in children is associated with correction in scoliosis; Reference : Natural history of scoliosis in children with syringomyelia, a retrospective review of 27 scoliotic patients with syringomyelia using MRI; Chiba University and Chiba Higashi Hospital, Japan; J Bone Joint Surg [Br] 2001;83-B:371-6; Received 9 February 2000; Accepted 19 April 2000.

Findings in intracranial haemorrhage

While reporting an intracranial bleed following finding should come in a proper order.

Site: Intra axial or extra axial as per classification. If intra axial mention about the anatomical area. If hematoma is sufficiently large and covering more than one anatomical site, first mention about the area which is its epicenter followed by other areas as its extensions. For this one need to know the basic anatomy. If extra axial try to differentiate between Epidural or Subdural.

Size or width: Size of the hematoma is major contributor in mass effect. Size of the hematoma calculated and mentioned in three dimenetions ie along all three axis. If not at least in two dimensions. Measurements must be tangential to each other. The best or ideal method is mentioning the volume of hematoma. In case of extra axial hematoma, whether its extra dural or sub dural, its maximum width is cranio cortical distance across the hematoma and tangential to hematoma.

Age: Acute, subacute or chronic. Mention about acute on chronic or sedimentation in hematoma. Membrane formation in case of SDH if any.

Density: mentioning density of hematoma as hyperdense, isodense or hypodense is better practice than acute, subacute or chronic which is relatively inaccurate. Its better to mention average attenuation value of hematoma in HU.

Perilesional odema:  mention about the amount of odema in terms of degree as mild, moderate and severe; because it contributes in mass effect.

Intra ventricular or subarachnoid space extension: mention in term of degree as mild, moderate and severe. An associated Ventriculomegaly, a known complication of intra ventricular extension and decides prognosis.

Mass effect : Mid line shift is length of a tangential drawn from midpoint of septum pellucidum on a mid line of bony calvarium, mentioned in mm. An associated internal herniation if any subfalcine, uncal or tonsillar herniation. Severity of mid brain compression in terms of mild, moderate or severe.

Any complication: Major intra cranial vessel compression and infarct secondary to internal herniations.

Comparison with the previous study if available: any progression or regression in size of hematoma, mass effect, intra ventricular bleed and Ventriculomegaly. If decompresive craniotomy , mention about changes in mass effect.

Intracranial hemorrhage

An intracranial hemorrhage is bleeding within the skull.
Occurs when a blood vessel within the skull is ruptured or leaks.
Can result from trauma as in head injury or non traumatic causes like hemorrhagic stroke secondary to hypertension, ruptured aneurysm, anticoagulant therapy or blood clotting disorders.
Itself a serious medical emergency as it can lead to raised intracranial pressure due to its mass effect and perilesional odema or can limit the blood supply of normal brain tissue. Internal herniations can lead to compression of vital brain structures.

Imaging modality:
CT scan ideal initial tool as it is definitive, accurate diagnosis, mass effect, cost effective, less time consuming for emergencies, suitable for non cooperative patients, easy availability, familiarity to new doctors on call,
MRI with Angiography for better evaluation in cases of non hypertensive haemorrhage to rule out underlying vascular malformation.

Broad classification: Intra-axial and Extra-axial.
Intra-axial haemorrhage: bleeding within the brain.
1. Intraparenchymal hemorrhage : bleeding within the brain parenchyma.
2. Intraventricular hemorrhage : bleeding within the brain's ventricles.

1. Intraparenchymal bleed further classified as basal ganglioinic and lobar bleed. Basal ganglionic are more common than lobar bleed, usually hypertensive. Lobar bleed are less likely to be hypertensive and other causes needs to ruled out.

2. Intraventricular hemorrhage are usually associated with or secondary to intra parenchymal bleed. Isolated intra ventricular bleed are rare.

Intra-axial haemorrhages are more dangerous and difficult to treat than Extra axial and are associated with further complications.

Extra-axial hemorrhage : bleeding that occurs within the skull but outside of the brain tissue.
1. Epidural hematoma : Between the skull and the dura.
2. Subdural hematoma : Between the dura and the arachnoid.
3. Subarachnoid hemorrhage: Between arachnoid and Pia.


Epidural hematoma (EPH)
98% cases associated with fracture; Post traumatic.
Involved vessel in tempero parietal region (Most common location) is Middle meningeal artery, In frontal region is anterior ethmoidal artery, in occipital region is transverse or sigmoid sinuses, in Vertex locus is superior sagittal sinus.
Lucid interval followed by unconsciousness.
Shape of collection is Biconvex or lentiform.
Surface area of hematoma smaller compared to sub dural, since limited by dural attachment at sutures.
Never cross suture lines.
May cross mid line falx in frontal region as its is outside the dura.


Sub dural hematoma (SDH)                            
Traumatic as well as non traumatic.
Involved vessels bridging veins.
Gradually increasing headache and confusion.
Shape of collection is concave or Crescent-shaped.
Surface area of hematoma larger , extend antero posteriorly over cerebral convexity.
Crosses suture line but never cross mid line.
May extend along interhemispheric fissure and tentorium.

Subarachnoid hemorrhage (SAH)

Besides from head injury may occur spontaneously, usually from a ruptured cerebral aneurysm.
Symptoms of SAH include a severe headache with a rapid onset ("thunderclap headache"), vomiting, confusion or a lowered level of consciousness, sometimes seizures.
CT is initial modality of choice seen a hyper density in the region of cortical sulci, basal cistern and sylvian fissure depending upon amount of bleed.
If CT is normal to be followed with MRI FLAIR and MR Angiography.
Confirmation is by lumbar puncture.

Meningitis as a delayed complication of head injury

A 23 yo male with history of admission for head injury ~ 6 month back, frontal lobe contusions and fractures of floor of anterior cranial fossa.
Now readmission for recent onset severe headache and neck stiffness, clinically signs of meningitis.
Immediate Post admission MRI Axial FLAIR image of Brain shows:

1. Focal cortical Gliosis involving frontal lobes near orbital surface more obvious on right side, possible secondary to previous head injury.
2. A focal dural thickening in left frontal region near floor of anterior cranial fossa.
3. Mild diffuse cerebral odema, T2 hyperintensity in the region of cortical sulci particularly in the dependent portions of brain suggestive of meningitis.
4. Marked mucosal thickening and collection ethmoid air cells.

A focal dural thickening in left frontal region near floor of anterior cranial fossa, mild diffuse cerebral odema, T2 hyperintensity in the region of cortical sulci in the dependent portions of brain suggestive of meningitis. An associated mucosal thickening and collection ethmoid air cells appears to be related to each other secondary to a possible fracture involving floor of anterior cranial fossa which may not be seen on MRI.

Conclusion: Meningitis as a delayed complication of head injury. 

POST TRAUMATIC MENINGITIS

Post-traumatic meningitis in head injured patients is uncommon, reported in 0.38-2.03%.

A skull fracture with accompanying dural tear results in a CSF fistula is typical, allows the subsequent passage of microorganisms into the cranial compartment. While CSF leak may resolve spontaneously, patients remain at risk for PTM as dural healing may be absent. Pneumocephalus which is seen in 86% of those with skull base fractures, is indicative of a dural tear with passage of air into the cranial cavity from an adjacent paranasal sinuses or mastoid. PTM has also been reported with fractures across infected paranasal sinuses, middle ear structures, and mastoid air cells without a dural tear.

Clinical presentation
The time between injury and diagnosis of PTM ranges from less than 24 hours to many years.
Signs and symptoms in PTM are variable. Fever (in 86-100%), deterioration in consciousness (in 97-100%) may be extremely rapid and progressive.
Triad of fever, stiff neck, and change in mental status.
Headache is also common (in 57-86%)

Causative agents for PTM include a wide range of both gram-positive and gram-negative organisms. Streptococcus pneumoniae is the most common agent and is isolated in 52-100% of cases. Other often reported gram-positive organisms include Staphylococcus aureus and streptococcal species.  Gram-negative organism encountered in 17-100% and is most often noted with open cranial wounds or lengthy hospitalizations. Commonly isolated gram-negative bacteria include Escherichia coli,  Klebsiella pneumoniae,  Neisseria meningitidis,  Haemophilus influenzae and Pseudomonas aeruginosa.
The diagnosis of PTM is usually made by CSF cultures. Cultures may fail to yield an isolate; negative cultures have been reported in up to 27% of cases.  The reason may be patient is already receiving prophylactic antibiotics.

Antibiotics should be chosen in accordance with the clinical situation and ability to penetrate the blood-brain barrier. Broad spectrum antibiotics are the choice.

Pneumonia, deafness, anosmia, mental retardation, or other major neurologic deficits are the common complications of PTM.

Miliary tuberculosis CNS

Miliary cerebral tuberculosis is one of rare menifestation of CNC Tuberculosis.
Involvement of CNS seen in approximately 5% of total patients of tuberculosis.
Usually due to hematogenous spread.
The variety of forms of involvement include tuberculous meningitis, tuberculomas, tuberculous abscesses, focal cerebritis, and the rarest one is miliary tuberculosis.
Miliary CNS tuberculosis is usually associated with tuberculous meningitis, a pathogenetic relationship is suspected between them.

At MR imaging appears as multiple tiny (< 2 mm), T2 hyperintense foci with nodular or ring enhancement on post contrast, disseminated through out supratentorium as well as posterior fossa. 

Insular ribbon sign in Acute Ischemia

The “Insular ribbon sign” is one of the early signs of acute MCA territory infarction.

In a set up with both CT and MRI, CT still remains the first imaging modality for initial evaluation of patients with suspected stroke. Lesions that clinically can mimic ischemic stroke, such as hypertensive hemorrhages  tumors complicated with bleed, complicated vascular malformations, and are to be excluded first. Once bleed is ruled out then pt can be subjected to MRI diffusion and other sequences to rule out acute stroke. This is a protocoal for stroke we follow. Reasons are cost effectiveness, less time consuming, suitable for non co operative patients, easy availability and relative familiarity of CT to the doctors on duty.
Most CT scans are negative in acute infarct in the first 6 hours after symptom onset.
However, several subtle parenchymal findings like insular ribbon sign can be sometimes seen and should be searched for.

The "insular ribbon sign" corresponds to blurring of the gray - white matter inter phase due to decreased attenuation of the gray matter which has undergone ischemia with an associated cytotoxic oedema  where normally the insular cortex and lentiform nucleus have slightly higher attenuation than the intervening external capsule. 

In this case,

CT attempted first, hypertensive bleed ruled out. 

Considering history of recent onset left sided weakness, there is subtle low attenuation of right insular region - insular ribbon sign positive. Immediate MRI Diffusion shows acute right MCA territory infarct, there is hardly any change on FLAIR except mild effacement of cortical sulci. MR Angiography of brain and neck show right MCA - ICA occlusion.

IVY sign in early infarction

History of 3hrs left side weakness. 

Axial FLAIR images of brain show abnormal serpigenous high signal along right cerebral convexity in peri sylvian region, normally not visualized due to flow voids represents cortical branches of right MCA with an abnormal very sluggish flow -"IVY" sign can be the early and only sign of acute ischemia. 

Brain parenchyma in the involved territory show normal signals.

Also reported in Vasculitis :  Post Tb Meningitis Vasculitis induced infarcts with "IVY" sign

Hyperdense MCA sign

The “Dense MCA or dense vessel sign” is one of the early signs of acute MCA territory infarction.

Corresponds to a hyperdense cord like MCA main stem in the Sylvian fissure on CT.

Represents thrombotic material in main stem of the MCA.

During such a hyper acute to acute stage of infarct the adjacent brain parenchyma in the involved territory may show normal attenuation pattern.

Dot sign in MCA thrombosis

The “Dot sign” is one of the early signs of acute MCA territory infarction.

Corresponds to a punctate hyperdensity on CT and hyperintensity FLAIR or T1w MRI images in the Sylvian fissure.

Represents thrombotic material in the M2 and M3 segments of the MCA. 

During such an acute stage of ischemia the adjacent brain parenchyma in the involved territory may show normal or faint high signal on FLAIR. The dot sign has a high specificity and high positive predictive value, but has low sensitivity.

Cord sign in CVT

Cerebral venous thrombosis (CVT) has variable clinical presentations.
Seventy-five percent of the CVT occur in young women, between 20 and 40 years of age, with the superior sagittal sinus (SSS) being most frequently affected (62% of cases).
Such increased incidence can be explained by pregnancy, puberty and use of oral contraceptives.
The diagnosis can be achieved by means of CT (the most readily available), magnetic resonance imaging (MRI) (the method of choice)
In 20% of cases, CT scans are normal.
CVT findings can be classified in direct and indirect.
The cord sign is a direct sign of CVT.
A focal vasogenic edema, infarction and hemorrhage are indirect signs.

"Cord sign" is a focal increased density on CT or a serpigenous low signal intensity on MRI T2*GRE due to thrombotic material in a vessel. 

The closest differential for this kind focal hyperdensity in the region of cortical sulcus on CT is sentinel sub arachnoid bleed and needs to be ruled out with MRI. 

Orbital subperiosteal hematoma

A 40 yo female with 3 month history of left orbital proptosis.

Left eye ball movement painful and restricted. 

No history of trauma.

Here is his MRI Brain Coronal T2, T1w images. Sagittal T1, axial T1w images.

This MRI study of brain shows:

A well demarcated lentiform shaped fluid signal intensity collection in superior quadrant of left orbit, hyperintense on T2, iso to hyperintense on T1.

No septations or loculations.

No destruction of adjacent orbital roof. 

Left orbital proptosis. 

Histopathology : Orbital subperiosteal hematoma

It's strange, an Orbital subperiosteal hematoma without history of trauma. The whole study reviewed again and revealed an associated adjacent ethmoid sinus mucocele. 

Orbital subperiosteal hematomas can develop associated with sinus infection. Such a condition should be treated as a sinusitis complication and the associated sinus infection must be treated concomitantly (Reference : Orbital subperiosteal hematoma associated with sinus infection; Rhinology. 2010 Mar;48(1):117-22; Park HW, Lee BJ, Chung YS)

Interhemispheric cyst without corpus callosal agenesis are usually Arachnoid

A 60 yo female with giddiness since 1 month.
Here is her MRI Brain; Coronal T2, Axial FLAIR, Coronal Post contrast T1, Diffusion and sagittal T1w images.

This MRI study of Brain shows:
A cyst along interhemispheric fissure on left side of falx, in left para sagittal parietal region, isointense to Csf, no restricted diffusion on diffusion. No adjacent parenchymal Gliosis or volume loss. Non enhancing on post contrast T1.
No associated corpus callosal malformation agenesis or dysgenesis on mid sagittal T1. Corpus callosum is compressed.
Cyst is not communicating with ventricular system. Left lateral ventricle compressed.

Imaging wise Possible DDs: Arachnoid cyst, Epithelial cyst.


In an elderly patient inter hemispheric cyst without associated corpus callosal agenesis are usually Arachnoid cysts. Whereas inter hemispheric cyst associated with agenesis of the corpus callosum, which will be clearly demonstrated on magnetic resonance imaging  are usually non arachnoid cysts.
Reference : 
1. Interhemispheric arachnoid cyst in the elderly: case report and review of the literature; Fumiyuki Yamasaki M.D,
2. A case of symptomatic interhemispheric arachnoid cyst in the elderly by M Tomabechi, K Takano, N Suzuki, G Daita.

Porencephalic cyst ruled out as there is no adjacent parenchymal Gliosis, volume loss or communication with ventricular system.
Epidermoid cyst ruled out as there is no restricted diffusion on diffusion.