Neuro Flashcards
Pt presents with severe HA during sex, what is most likely?
Benign mesencephalic SAH: –have to r/o aneurysm obvi but this can be done w/2 negative CTAs or angiograms
72M p/w headache and left sided weakness
Subacute SDH
isodense or hypodense to the underlying cortex.
may be difficult to appreciate on NECT
Fx that help in making the correct diagnosis: medial displacement of the gray-white matter junction, sulcal effacement, and subfalcine herniation
Subdural hygroma is 2/2 tearing of dural bridging veins and is isodense to CSF.
Acute subdural hematoma is homogeneously hyperdense or mixed hyper and hypodense if active bleeding.
25 year old involved in MVA
Chance fracture is characterized by a vertebral body wedge compression and anterior displacement of the spine above the fracture with facet subluxation. It may involve primarily soft tissues and extend through disc and interspinous ligaments. This is a 3 column injury.
49F w/right neck mass
Post Con T1
Carotid Body Paraganglioma
—An intensely enhancing soft tissue mass that splays the carotid vessels at the bifurcation is unlikely to be anything but carotid body paraganglioma. In this particular case, only subtle high velocity flow voids are present as a result of the small size of the lesion.
—A glomus vagale Paraganglioma would be about 2 cm below the skull base in the nasopharyngeal portion of the carotid space, whereas in this case the mass is lower, at the level of the bifurcation
—Neurofibroma could be seen here but would displace and not splay the vessels, also would have poor enhancement
—Schwannoma could be seen in carotid space and enhance brightly but NO flow voids and would displace vessels anteromedially not splay them
50F with HA
Post-con T1
Metastatic disease
Enhancing, infiltrating lesions in the scalp and skull with adjacent dural-based masses in a middle-aged/older adult should be considered metastatic disease until proven otherwise. The withheld history in this case is known breast cancer with systemic metastases.
—Multiple meningiomatosis would not be so diffuse
—Extramedullary Hematopoiesis can give multiple dural based masses, again not as diffuse and dx would include chronic anemia or PV etc
—Neurosarcoid would not involve the skull and scalp (same w/Rosai Dorfman-although can see the dural stuff w/sinus histiosis w/massive LAD)
45F after MVA develops hydrocephalus. What is the cause?
the most common cause of extraventricular obstructive (noncommunicating) hydrocephalus is SAH which is present here—> SAH stops resorption of CSF from arachnoid granulations and it builds up in vents
(This patient also has IV hemorrhage but it is not obstructing) Intraventricular hemorrhage can cause communicating hydrocephalus due to obstructed cerebrospinal fluid (CSF) resorption at the level of the basal cisterns or arachnoid granulations. It is important to recognize hydrocephalus in the setting of intraventricular hemorrhage, as these patients may require urgent CSF diversion (shunt)))
38M w painless ptosis and optic neuropathy
heterogenous enhancement on post-gad T1
Coronal STIR
Cavernous Hemangioma
Cavernous hemangioma is the most common adult orbital mass lesion. Actually a vascular malformation, this lesion is typically very well defined with a dynamic filling-in pattern of intense enhancement.
—>lymphoma in the orbit would be infiltrating and encase the structures or invade-not discrete like this
—> hemangiopericytoma is not usually seen in the orbit, and is usually infiltrative but CAN look like this RARELY
—> orbital meningioma would be tubular along the optic nerve sheath and may calcify
—> orbital varix would be vascular channels and pt would have sensation of fullness w/Valsalva
pt w/ back pain.
Scheurmann disease
Dx depends upon 3 contiguous disc levels having the following abnormalities:
(1) Mild anterior wedging (≥ 5 degrees)
(2) endplate irregularity
(3) Schmorl nodes
(4) kyphosis.
Back pain is the typical symptomatic presentation, with many cases being incidental and asymptomatic.
12F w/progressive upper extremity weakness over 48h
findings in this case are highly suggestive of tumefactive demyelination. The incomplete rim of “horseshoe” enhancement , with the “open” (nonenhancing) part of the “horseshoe” facing the cortex, is a classic imaging finding for demyelinating disease (not abscess or glioblastoma).
—> she was subsequently dx w MS
33M w few days of HA, Fever, malaise p/w seizure
Herpes encephalitis
The bilateral but somewhat asymmetric cortical and subcortical FLAIR hyperintensity in the medial temporal and inferior frontal lobes and insula indicates limbic system involvement and is therefore almost surely herpes encephalitis
—> limbic encephalitis could look like this too but would be older patient w/o hx of infection, more chronic.
57F w/HA and lump on head
: In a middle-aged or older patient, metastasis would be (by far) the most common cause of scalp+skull+dura/epidural mass. Everything else (osteomyelitis and primary diploic space lesions, such as intraosseous meningioma) would be rare. As it turned out, this patient had a remote (REALLY remote) history of thyroid cancer.
Most skull metastases are osteolytic. classic “culprits” are lung, renal, thyroid, and breast primary sources. While there are lots of pathologies that can cause both solitary and multiple lytic calvarial lesions, not too many also involve the subgaleal soft tissues, epidural space, and dura. Infection can but is much less common than metastatic disease. There is a bimodal distribution for skull metastases. A smaller peak in children (medulloblastoma, leukemia, neuroblastoma) and a larger (MUCH larger) peak in adults.
Retinoblastoma
At lease 90% show calcifications intratumorally which are finely speckled or flocculated in appearance.
6 year old with progressively enlarging right cheek mass
Rhabdomyosarcoma
Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children and can occur anywhere in the head and neck, such as this mass arising in the masticator space. RMS presents as a soft tissue mass, with bone changes that vary from nonaggressive bone remodeling, as seen in this case, to aggressive osseous destruction.
LCH presents as uni- or multilocular lucent lesions with bony changes and soft tissue mass. However, unlike the remodeled appearance of bones in this case, LCH shows sharply marginated lucent bony lesions, sometimes described as having “beveled edges.”
Intra-axial tumors generally arise from glial cells and are named after their cell type components—> while extra-axial tumors arise from non-glial cells :give some examples
Intra-axial:
Astrocyte—> astrocytoma
Oligodendrocyte—> oligodendroglioma
Ependymoma—> ependymoma
Choroid plexus—>choroid plexus tumors
Extra-axial:
Meningioma, Hemangioblastoma, sarcomas, lymphomas, etc.
Blown pupil is classic for which herniation?
Uncal herniation(effacement of CN III)
will see effacement of ambient cistern and contralateral hydrocephalus
Most common site for hypertensive IC hemorrhage?
Putamen/External capsule
followed by thalamus
then pons/cerebellum
then lobar
Third Occipital Condyle
May articulate with dens
—>is continuous w/foramen magnum
Teen w/several days increasing HA
Meningitis
Both basilar cisterns are completely effaced and appear filled with ill-defined, mildly hyperdense material . The right temporal horn is enlarged , suggesting early obstructive hydrocephalus. The substance that fills the basilar cisterns is not sufficiently hyperdense for blood. This looks like a thick exudate and is most consistent with meningitis. Tuberculosis and coccidiodomycosis are notorious for causing thick, dense exudates that preferentially involve the basilar cisterns.
Zygomaticomaxillary complex fractures (tripod fx) involves which bones
Zygomatic arch, lateral orbit, maxillary sinus
—> maxillary component can be subdivided
Enthesioneuroblastoma
Esthesioneuroblastoma is a malignant tumor of the olfactory mucosa that is centered in the high nasal cavity. It spreads early along the olfactory nerve into the anterior cranial fossa. When discovered, it most commonly has a “snowman” configuration with its waist in the area of the cribriform plate, a superior lobule in the floor of the anterior cranial fossa, and an inferior lobule in the high nose and ethmoid sinuses. Marginal intracranial cysts may be seen with this tumor. Bone CT shows central anterior skull base destruction early. Avid enhancement on MR.
—>Sinonasal undifferentiated carcinoma (SNUC) is also rapidly progressive but usually invades the orbits as well. If ONLY goes up it can mimic
—>Sinonasal non- Hodgkin Lymphoma usually causes more remodeling, less cortical destruction and rarely spreads into the anterior cranial fossa. Homogenous enhancement
—> Sinonasal Squamous cell Carcinoma (SSCC) usually begins in maxillary antrum and spreads to involve nose secondarily. If it were to start in nose and spread superiorly (would be rare) could mimic
Causes of leucocoria
Retinoblastoma—can calcify
Coats disease—doesn’t calcify (exudative retinitis/associated w VATER syndromes-V shaped exudate can look similar to retinal detachment )
PHPV—persistant fetal vasculature (in posterior form, small globes and can get retinal detachments, triangular shaped)
Cerebriform
Inverted papilloma
benign neoplasm
CPA angle mass (vestibular aqueduct) with erosion of bone and high T1, heterogenous T2 w/enhancement of cystic part of tumor
Endolymphatic sac tumor
Think VHL for these
ddx includes glomus jugulare, cholesterol granuloma, petrous apicitis, and enlarged aqueduct
Few days of BL lower extremity weakness
Guillan Barre Syndrome
Diffuse, smooth enhancement of the nerve roots
30 something woman on OCPs
Dural Venous Sinus thrombosis
Commonly in women, esp on OCPs
Direct: thrombus (dense clot sign, emtpy delta sign…) look for lack of flow voids in the sinuses on T1, T2, FLAIR)
Bilateral vertebral artery dissection
sickle shaped hyperintensity in vessel wall (T2 FS MR images best)
Central Neurocytoma
WHO Grade II neuroepithelial intraventricular tumor—> heterogenous mass w/variable size and enhancement, 50% in lateral ventricles near foramen of Monroe, usually attached to septum pellucidum
Calcification and intratumoral hemorrhage common
ddx includes meningioma, ependymoma (MC 4th vent in a child), subependymoma, subependymal GCA (tuberous sclerosis)
Gliomatosis Cerebri
Infiltration glial tumor involving at least three lobes, must have gray matter involvement. Involved structures are enlarged and cause mass effect
usually do not enhance
Medulloblastoma
>90% in cerebellum, most in vermis.
small round blue cell tumors
Heterogenous enhancement. Hypo on T1, iso on T2/FLAIR, restrict on DWI
4 types/A/w multiple syndromes/
Primary CNS Lymphoma
MC in >50
historically a/w HIV/AIDS and EBV/immunocompromised
60-70% are single lesions w/predeliction for periventricular WM
classically hyperdense avidly enhancing mass, low T1, iso-hyper T2, restricting, cross corpus callosum
HIV patient
toxoplasmosis
usu multiple, rim enhancing lesions
favors basal ganglia, thalami and corticomedulary jctn
may have central mural nodule, may have calcification
LeFort I = floating palate
LeFort II = pyramidal fracture
LeFort III = craniofacial dissociation
What are you worried about/looking for?
Necrotic conglomerate nodes in level II—> look for SCC of the palatine tonsil specifically
Any necrotic/conglomerate nodes in the neck—inspect waldeyer’s ring
Benign mixed tumor doesn’t cause these kind of nodal conglomerates, and lymphoma doesn’t usu have necrotic nodes.
Multiple LP attempts, unsuccessful. This MR afterwards
Traumatic subdural hematoma
epidural fat is intact making it in subdural space
—> can be lenticular or lobulated with ‘cinched’ appearance of nerve roots
Severe Cerebral Edema with Hypoxic Ischemic Encephalopathy
—> the brighter Sylvain fissures and interhemispheric fissure are 2/2 to hypodensity of swollen cerebrum NOT SAH
—> Cerebellum/posterior fossa are spared initially and appear normal here (white cerebellum sign)
Hemorrhagic stroke
Hypertensive hemorrhage 2nd MC type of stroke, and HTN is 2nd MCC of IC hemorrhage in 45-70 year olds
—> MC basal ganglia, thalami, pons, and cerebellum
—> AVMs typically present earlier in life (also calcs, vessels)
—> AMyloid angiopathy can cause hemorrhage, usu lobar
Cervical Spondylosis
—> effaced CSF in the C spine at disc levels. Can get cord edema or myelomalacia
—> insidious onset, periods of static disability and episodic worsening
Calcific Tendinitis of the Longus Colli
*most important point is not to confuse for retropharyngeal space abscess
Segments and branches of vertebral arteries?
V1: segmental cervical muscular and spinal branches
V2: anterior meningeal artery, muscular and spinal branches
V3: posterior meningeal artery
V4: anterior and posterior spinal arteries (ASA and PSA), perforating branches to medulla, posterior inferior cerebellar artery
34M with progressively altered mental status
Upward transtentorial herniation
—notice the intact third and lateral vents but NO 4th—> Inspect the posterior fossa for a mass and upward herniation
Chance fracture
splitting of pedicle into superior and inferior parts as well as horizontal fracture line—flexion distraction injury/chance fracture
(other pattern of chance fracture is anterior superior spine dislocation with facet subluxation//jumped or perched facet
Classic for what?
Chronic hypertensive encephalopathy—-> multiple hypertensive strokes
blooming black dots on SWI/GRE/T2* images in cerebellum and deep gray structures (supplied by perforators)
—> amyloid angiopathy usually affects cortex and pia. Here can also look for evidence of old SAH and siderosis (rare in chronic HTN)
What are CT and MR findings in Hypoxic Ischemic Encephalopathy?
CT— hypointense cortex and basal ganglia
MR—restricted diffusion early f/b T2 hyperintensity in Basal ganglia, cortex. Can get watershed infarcts also
Cystic lesion with enhancing mural nodule in a young patient with hx of seizure
Ganglioglioma\
WHO I-II mixed glial/neuronal tumor
MC neoplastic cause of temporal lobe seizures
Petrous apex lesion with smooth expansile margins on CT and ^ T1 and T2 on MR
Cholesterol Granuloma
2/2 repeat intralesional hemorrhage– in surg, find a cyst with old blood
T1 ^ from methemoglobin and T2 ^ from methemoglobin and hemosiderin
*Cholesteatoma can mimic on CT but on MR has LOW T1 signal
Holoprosencephaly
-spectrum of failed forebrain cleavage
least severe= lobar
most severe = alobar: monoventricle, thalamic fusion, w/forebrain fusion can have single ACA (azygos artery) on MRA
can get proboscis with single nasal opening, cleft palate, (face predicts the brain)
fever and pain
Ludwig Angina
radpidly progressive floor-of-mouth infection
3 F’s :feared, often fatal but rarely fluctuant
Cholesteatoma
histologically-equivalent to an epidermoid cyst and are composed of desquamated keratinizing stratified squamous epithelium
Restrict diffusion**
thunderclap HA, in a woman (may be pregnant)
RCVS
(thought to be 2/2 decreased progesterone when in pptm patients)
Imaging: can be normal, esp early.
directly visualized multiple stenoses, +/- complications related to stenoses such as watershed infarcts, SAH, lobar hemorrhage, vasogenic edema
Pt p/w HA, seizure, encephalopathy
PRES
Acute hypertensive encephalopathy-HTN and/or related endothelial dysfunction
Seen in: severe HTN (preeclampsia), drug toxicity (cisplatin, cyclophosphamide..), SLE, HUS, TTP, etc
Imaging: holohemispheric at watershed zones, superior frontal sulcus, and parieto-occipital predominance
–T2 WMH on MRI, variable enhancement (hypo on CT)
Dural venous sinus thrombosis
often bilateral and hemorrhagic
also think of when you see temporal lobe infarct, cortical edema/hemorrhage, peripheral lobar hemorrhage
thickened, nodular pituitary stalk
Lymphocytic/autoimmune hypophysitis
often pptm or 3rd trimester, F>M
anterior more common, mimics adenoma, common hormone deficiencies
posterior rare, get diabetes insipidus,
Usually self limited
Wernickes encephalopathy
thiamine (B1) deficiency
mostly alcoholics, sometimes a/w morning sickness in pregnancy, p/w opthalmoplegia,ataxia, and confusion
enhancment in mamillary bodies (T2 bright along thalami and periaqueductal gray)***
chronically, can evolve into korsakoff syndrome, c/b confabulation and global amnesia
Progression of NMA//neuronal migration
- First set of neurons form in germinal matrix (schizencephaly) (2 layer cortex)
- Neuroblasts proliferate in germinal matrix (gray matter heterotopia-nodular)
- Neuroblasts migrate towards the exterior (pial) surface (gray matter heterotopia-laminar)
- Daughter Neuroblasts separate from the superficial tips and migrate towards the surface (creating the LAYERS) (Agyria/Pachygyria)
- Superficial layer involutés and cortex organizes (polymicrogyria)
