Neuroimaging in Seizure

IMAGING MODALITIES USED IN SEIZURES

1. CT Scan
2. MRI (and advanced MRI techniques s.a. DTI, magnetization transfer imaging, voxel-based analysis, T2 mapping) and functional MRI (fMRI)
3. PET Scan
4. SPECT Studies
5. magneto encephalography / magnetic source imaging

CT Scan
– to exclude acute neuro problems that require urgent intervention
– hemorrhages, gross structural malformations, large tumors, calcified lesions

7 Structural Causes to look for in MRI:

1. Mesial temporal sclerosis
2. Cortical dysplasia
3. Brain tumors
4. Vascular malformations
5. Cerebral infarction / hemorrhage
6. Traumatic brain injury
7. Infections (encephalitis, cerebral access, granulomas, cysts)

MESIAL TEMPORAL SCLEROSIS
– AKA hippocampal sclerosis
– most commonly diagnosed structural abnormality in epilepsy
– presents in childhood
– surgery is curative
– MRI characteristics: hippocampal atrophy , increased t2 and flair signal intensity
– look for MRI changes in coronal T2W images and coronal FLAIR

Figure.  Subtle gliosis of left hippocampus (blue arrow) and atrophy (yellow arrow).

CORTICAL DYSPLASIA
– second most common structural etiology for epilepsy
– lesions congenital, usually presents in childhood

MRI findings suggestive of cortical dysplasia

1. cortical thickening
2. blurring of gray-white margin
3. increased signal on FLAIR
4. subtle tapering bands of gray matter extending from the cortex towards the ventricles

Brain tumors and cerebrovascular disease
– more common in elderly

NEUROCYSTICERCOSIS
– caused by Taenia solium
– common etiology in endemic populations (Mexico, Latin America, Russia, India, Pakistan, Southeast Asia, China, West Africa)
– MRI with contrast, but CT is more sensitive for detecting small areas of calcification

Note: most individuals with new onset epilepsy will not have a structural lesion on MRI, yield is 14%.

EPILEPSY PROTOCOL:
– Standard T1-weighted images
– T2 weighted fast spin echo sequences
– Gradient echo sequences
– FLAIR sequences
– 3d volume acquisition sequences with high def of grey-white junction including magnetization prepared rapid acquisition gradient-echo (or MP RAGE), 3-D fast spoiled gradient recalled echo acquisition at steady state (or 3-D fast-spoiled GRASS or 3-D SPGR)

Note: MRI evidence of hippocampal atrophy is a strong predictor of excellent postoperative seizure control after anterior temporal lobectomy.

Advanced MRI techniques
– high field strength MRI: 3 Tesla
– use of multichannel phase array surface coils
These techniques allow for a higher signal to noise ratio, improved imaging uniformity, and better spatial resolution.

DIFFUSION TENSOR IMAGING (DTI)
– reveals white matter tracts
– delineate epileptogenic substrate and surrounding tissue

SUSCEPTIBILITY-WEIGHTED IMAGING (SWI)
– exploits magnetic properties of blood or hemosiderin
– more sensitive in detecting cavernous malformations
– identifies epileptogenic, post-infectious, calcified lesions eg Cryptococcus, tuberculosis, cysticercosis

MRI findings that are not known to be epileptogenic:

1. punctate  foci of T2 signal change in the white matter
2. many cystic lesions such as arachnoid cysts, choroidal fissure cysts
3. lacunar strokes
4. ventricular asymmetry
5. diffuse atrophy
6. isolated venous anomalies

MRI changes after seizures

1. local swelling
2. increased T2 signal intensity
3. restricted diffusion
4. focal and/or leptomeningeal contrast enhancement

FUNCTIONAL MRI

• detect focal changes in blood flow and oxygenation levels that occurs when an area of the brain is activated
• change in neuronal activity accompanied by change in ratio of oxy to deoxyhemoglobin in blood
  measured as the blood-oxygen-level-dependent (BOLD) effect
• used to noninvasively map motor, sensory and language functions; surgical planning
• may eventually replace carotid amobarbital (Wada) test for language lateralization
• *Powerpoint show: fMRI simplified <linkout>

PET SCAN

• 2[18f] fluoro-2-deoxy-d-glucose positron emission tomography or FDG-PET
• images topographic distribution of glucose uptake in brain
• provides a picture of brain metabolism
• performed in interictal state
• goal is to detect focal areas of decreased metabolism (functional disturbances of cerebral activity associated with epileptogenic tissue)
• sensitivity increased when seizures are more frequent or performed soon after seizure has occurred

PET scan. The arrow points to where the seizures are coming from.

SPECT STUDY

• single photon emission computed tomography study
• radiolabeled tracer (99mTc-hexamethylpropyleneamineoxime or 99mTc-HMPAO) injected which binds on first-pass through brain
• provides snapshot of cerebral circulation
  • ictal SPECT – shows hyperperfusion at seizure focus with surrounding hypoperfusion
  • post-ictal and interictal SPECT – shows regional hypoperfusion
• SISCOM (subraction ictal SPECT scan coregistered with MRI) improves localization
• limitations: injection timing is critical

Ictal SPECT perfusion exam demonstrates a hyperperfused (metabolic) area in the right temporo-parietal region which corresponds to a hypoperfused region on the inter-ictal exam. 

MEG/MSI

• magnetoencephalography (MEG) and magnetic source imaging (MSI)
  • MEG – recording of magnetic fields generated by intraneuronal electrical currnets
  • MSI – combination of MEG source localization with coregistered anatomical imaging in which magnetic dipole representing an epileptiform discharge is placed on patient’s MRI scan
• approved for presurgical localization for epilepsy and for localization of neuronal function

References

AuntMinnie.com,. ‘SPECT Imaging In Seizure Disorders Discussion’. N.p., 2015. Web. 27 Sept. 2015.

Radiologyassistant.nl,. ‘The Radiology Assistant : Role Of MRI In Epilepsy’. N.p., 2012. Web. 26 Sept. 2015.

Seattlechildrens.org,. ‘Epilepsy Symptoms And Diagnosis | Seattle Children’S Hospital’. N.p., 2015. Web. 26 Sept. 2015.

Slideshare.net,. ‘Fmri Terms: HRF And BOLD’. N.p., 2015. Web. 26 Sept. 2015.

Uptodate.com,. ‘Neuroimaging In The Evaluation Of Seizures And Epilepsy’. N.p., 2015. Web. 26 Sept. 2015.

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Post-operative Supplementary Motor Area Syndrome

Supplementary motor area (SMA):

• important in programming and initiating complex motor sequences involving bilateral hand coordination, postural preparation and distal extremity movement

Three Stages:

1. global akinesia that is worse contralaterally
2. sudden recovery a few days later, but with a persistent reduction in contralateral motor activity
3. subtle sequelae within weeks to months after surgery

Types:

1. Complete SMA syndrome – as contralateral hemiplegia with or without mutism
2. Partial SMA syndrome – contralateral hemiparesis and/or speech hesitancy

CLINICAL PRESENTATION:

• reduction of spontaneous movements and difficulty performing voluntary motor acts to command contralateral limbs
• tone in the limbs is maintained or increased
• serial automatic motor (like walking) activities are relatively unaffected
• speech deficits may be seen
• hemineglect and dyspraxi or apraxia involving contralateral limbs

PROGNOSIS:

• usually recover motor function over a variable  time period from one to a few weeks
• good long-term prognosis

Proposed mechanisms of modulation of the SMA in normal subjects, SMA syndrome, PD and tics.

The SMA can both positively and negatively modulate the contralateral SMA. In normal conditions this tonic interhemispheric balance may result in both initiation and inhibition of movements.

In the SMA syndrome this balance is disturbed, leading to temporary lack of movements (akinesia) of the contralateral limbs and irreversible deficits of bimanual alternating movements. The functional schemes are projected on a coronal MNI brain section. = denotes unchanged modulation, < denotes decreased modulation, > denotes increased modulation.

References

Ryu, Ju Seok, Min Ho Chun, and Dae Sang You. ‘Supplementary Motor Area Syndrome And Flexor Synergy Of The Lower Extremities’. Ann Rehabil Med 37.5 (2013): 735. Web. 24 Sept. 2015.

Front. Hum. Neurosci., 28 November 2014 | http://dx.doi.org/10.3389/fnhum.2014.00960.  Insights from the supplementary motor area syndrome in balancing movement initiation and inhibition. A. R. E. Potgieser, et al.

SMASH U Classification of ICH

A simple and practical clinical classification for the etiology of intracerebral hemorrhage from Helsinki University Central Hospital.

SMASH U stands for:

• (S) structural vascular lesions – including cavernomas and AVMs – 5%
• (M) medication – 14%
• (A) amyloid angiopathy – 20%
• (S) systemic disease (liver cirrhosis, thrombocytopenia, others) – 5%
• (H) hypertension – 35%
• (U) undetermined – 21%

*patients with structural lesions have smallest hemorrhages and best prognosis; anticoagulation-related ICH were largest and most often fatal.

REFERENCE:  

Stroke. 2012 Oct;43(10):2592-7. Epub 2012 Aug 2.  SMASH-U: a proposal for etiologic classification of intracerebral hemorrhage.  Meretoja A., et al.

Chiari Malformations

DEFINITION:  heterogeneous group of disorders that are defined by anatomic anomalies of the cerebellum, brainstem, and craniocervical junction, with downward displacement of the cerebellum, either alone or together with the lower medulla, into the spinal canal

NOTES:  

• normal cerebellar tonsils may lie up to 3 mm below the foramen magnum in adults.
• tonsils lying 5 mm or more below the foramen magnum on neuroimaging are considered to be consistent with a Chiari malformation
• With infants, however, tonsils as low as 6 mmbelow the foramen magnum can still be normal.
• there is no direct correlation between how low the tonsils are lying and clinical severity.
• Chiari malformations are associated with spinal cord cavitations (ie, syringomyelia).

Table.  Classification of Chiari Malformation.

Type	Description
Chiari 0	anatomic aberration of the brainstem (posterior pontine tilt, downward displacement of the medulla, low lying obex) but with normally placed cerebellar tonsils
CM-I	abnormally shaped cerebellar tonsils that are displaced below the level of the foramen magnum
Chiari 1.5	CM-II like malformation without spina bifida
CM-II	downward displacement of the cerebellar vermis and tonsils, a brainstem malformation with beaked midbrain on neuroimaging, and a spinal myelomeningocele
CM-III	small posterior fossa with a high cervical or occipital encephalocele, usually with displacement of cerebellar structures into the encephalocele, and often with inferior displacement of the brainstem into the spinal canal
CM-IV	cerebellar hypoplasia unrelated to the other Chiari malformations

Bony Abnormalities seen in CM:
●Atlas assimilation – common in CMI
●Atlantoaxial dislocation
●Klippel-Feil anomaly (congenital anomaly consisting of failure of segmentation of any two of the seven cervical vertebrae)
●Platybasia deformity where lower occiput is pushed by upper cervical spine into cranial fossa
●Basilar invagination -(protrusion of the odontoid process through the foramen magnum into theintracranial cavity)
●Luckenschadel, also known as lacunar skull; ossification disorder in which the fetal skullappears fenestrated
Other findings in CM-II
●Inferior displacement of the fourth ventricle into the upper cervical canal
●Elongation and thinning of the lower pons and the medulla
●Beaking of the quadrigeminal plate
●Kinking of medullary spinal cord junction in the cervical canal
●Stenosis or atresia of the cerebral aqueduct
●Upward displacement of the upper cerebellum into the middle fossa
●Cerebellar dysplasia
●Colpocephaly (abnormal enlargement) of the posterior lateral ventricles

Theories on Pathogenesis:

1. MOLECULAR GENETIC THEORY – genes that program hindbrain segmentation and bone growth is defective
2. CROWDING THEORY – growth of posterior fossa is restricted causing compression of brain and squeezes contents through foramen magnum
3. HYDRODYNAMIC PULSION THEORY – early hydrocephalus (as fetus) pushes cerebellum and brainstem down
4. OLIGO-CSF THEORYneural tube does not close, causing CSF leak; insufficient CSF to distend ventricles which leads to disorganization
5. TRACTION BY TETHERED CORD – tethered cord pulls on cerebellar tissue

Pathogenesis of Spinal Cord Cavitations (Syringomyelia)

• CSF forced into central canal due to impaired subarachnoid circulations
• craniospinal pressure dissociation due to blocked CSF flow which leads to pressure backup into venous system, engorgement of Virchow-Robin spaces.  Excess fluid leads to spinal cord edema.  Fluid accumulation beyond resorptive power of parenchyma and dissipates into central canal and dilates it leading to syrinx formation

Presyrinx – potentially reversible; spinal cord edema due to obstruction of CSF flow, often in cervical region; appears similar to true syrinx on T2 but lacks discrete cavitation on T1

A diagrammatic representation of CSF flow under normal circumstances.

A: Sagittal view of the craniocervical junction and upper cervical spinal cord in an anatomically normal patient shows no obstruction to CSF flow at the foramen magnum. A segment of spinal cord parenchyma (box) is shown in more detail in part B.

B: Magnified view of the box in part A shows CSF flow dynamics in a normal patient with a variably stenotic central canal (CC), as indicated by the horizontal lines. CSF pressure (vertical arrow) is normal. CSF flows from the subarachnoid space (SAS) between the arachnoid (A) and pia (P) to the subpial space, and then enters the perivascular space (PVS). CSF circulates through the cord parenchyma toward the central canal, but may also flow in reverse as these forces are relatively balanced under normal circumstances (double-headed arrows).

Diagrammatic representation of syringomyelia and the “presyrinx” hypothesis in the setting of obstruction to CSF flow.

A: Sagittal view of the craniocervical junction in a patient with a Chiari I malformation shows abnormal descent of the cerebellar tonsil below the level of the foramen magnum(arrow). A segment of spinal cord parenchyma (box) is magnified in parts B to D, which represent views of CSF dynamics at the level of the spinal cord parenchyma in the presence of alterations in normal CSF flow and variable patency of the central canal.

B: Focal noncommunicating syrinx. In the setting of a Chiari I malformation and a variably stenotic central canal (which is a normal variant in many adults), as the tonsils descend rapidly during systole, CSF is driven into the spinal cord parenchyma by increased CSF pressure (thick vertical arrow). Net CSF flow occurs toward the central canal, resulting in focal syringomyelia which is limited in its craniocaudal extent by intervening stenosis of the central canal. CC = central canal, A = arachnoid, P = pia, SAS = subarachnoid space, PVS = perivascular space.

C: Extensive noncommunicating syrinx. This situation is similar to B, but the central canal is more extensively patent. In this situation, a long-segment dilation of the central canal (curved arrows) occurs as CSF is driven into the central canal via the perivascular spaces by the accentuated CSF pulse pressure (thick vertical arrow) that results from downward motion of the low-lying cerebellar tonsils in systole.

D: “Presyrinx”. In the setting of altered CSF flow, as with a Chiari I malformation, fluid in the subarachnoid space is subjected to increased pressure (thick vertical arrow). Net CSF flow is into the spinal cord parenchyma; however, because the central canal is not patent (as indicated by thehorizontal lines), fluid cannot accumulate within the central canal (curved arrows) and therefore diffuses through the cord parenchyma (stippled area),resulting in cord enlargement.

Diagnosis:

• MRI is best modality
• CT hig res if MRI cannot be performed
• fetal US?
• Cine phase contrast MRI – studies the flow across foramen magnum (determine need for surgery)
• polysomnography – if with sleep apnea, to determine if central or peripheral

Important anatomic / radiologic landmarks:

TREATMENT:

1. posterior foramen magnum decompression with or without dural opening
2. anterior foramen magnum decompression – transoral odontoidectomy
3. shunting procedures

References

Medscape,. ‘The ‘Presyrinx’ State’. N.p., 2015. Web. 24 Sept. 2015.

Uptodate.com,. ‘Chiari Malformations’. N.p., 2015. Web. 24 Sept. 2015.

Lovenox Reversal

– Discontinue Lovenox
– If significantly excessive dose given,  administer protamine
– aPTT remain prolonged to a greater extent than seen in UFH
– Anti-factor Xa never completely neutralized

Neutralization of enoxaparin by protamine
-Last dose given 8 hours and ≤ 12 hours=0.5 mg protamine per 1mg enoxaparin
– ≥ 12 hours=may not be required

A second infusion of 0.5 mg protamine per 1 mg LOVENOX may be administered if the aPTT measured 2 to 4 hours after the first infusion remains prolonged.

Watch out for:
severe hypotensive and anaphylactoid reactions

*LMWH reversal
[8h since last LMWH dose]
Dose: 0.5 mg IV per 100 anti-Xa units LMWH; Max: 50 mg/dose; rate 5 mg/min; Info: may repeat dose x1 if bleeding continues; protamine incompletely neutralizes LMWH effects; 1 mg enoxaparin = 100 anti-Xa units

ionically binds heparin, forming a stable complex which neutralizes anticoagulant effects

Anterior Cerebral Artery

Illustration demonstrating segments and branches of ACA and location of A3As.

Illustration demonstrating segments and branches of ACA and location of AdistAs.

Microsurgical division of DACA aneurysms with emphasis on AdistAs.

References

Lehecka, Martin et al. ‘Microneurosurgical Management Of Aneurysms At A3 Segment Of Anterior Cerebral Artery’. Surgical Neurology 70.2 (2008): 135-151. Web. 20 Sept. 2015.

Lehecka, Martin et al. ‘Microneurosurgical Management Of Aneurysms At A4 And A5 Segments And Distal Cortical Branches Of Anterior Cerebral Artery’. Surgical Neurology 70.4 (2008): 352-367. Web. 20 Sept. 2015.

Pituitary Region Masses (differential diagnosis)