Examination Protocols and Strategies
The necessity of imaging and selection of examination modality are primarily dependent
on the expected symptom cluster. Additional factors may also include local availability
of different examination modalities, the age of the patient and general clinical situation,
such as accompanying unconsciousness.
In every case, imaging is indicated in the presence of red flags, including appearance
of headaches in cancer or HIV-positive patients, if headaches first appear in a patient
after 50 years of age as well as headaches with increasing intensity, accompanying
systemic reaction such as fever or focal-neurological deficit [5]
[6].
In emergency situations when patients have potentially life-threatening causes, e. g.
in cases of subarachnoid hemorrhage or headache with accompanying unconsciousness,
CT is the preferred diagnostic method due to the shorter examination time as well
as better access to the patient and easier monitoring of the patient during the examination.
A CT-based examination protocol ([Table 2]) should include a non-enhanced CT with an orbital-meatal angulation from the base
of the skull to the vertex. This can use a sequential technique as well as a spiral
CT with newer equipment. Image data should be reconstructed in the soft tissue and
bone window.
Table 2
Basic examination protocol for CT and MRI in cases of headache.
|
CT
|
|
|
technique
|
indication/attribute
|
|
Non-enhanced CT
|
exclude hemorrhage, mass, infarction
|
-
incremental CCT with orbital-meatal layer orientation
-
4.5 mm slice thickness, supra- and infratentorial
-
reconstruction in soft tissue and bone window
|
|
arterial CT angiography (CTA)
|
caudocranial scan direction, 60 ml contrast agent with 4/6 ml flow rate, semiautomatic
bolus tracking at cervical vertabrae 5/6; scan region aortic arch to vertex
|
|
venous CT angiography (CTV)
|
craniocaudal scan direction; 80 ml contrast agent with 3 ml flow rate, 45 sec scan
delay
|
|
contrast-enhanced CCT
|
primarily for infectious process, tumor
|
|
MRI
|
|
|
technique
|
indication/attribute
|
|
|
|
T1w
|
anatomy, exclude hemorrhage, mass; if possible, as 3 D T1w MPR, otherwise axial T1w
|
|
DWI
|
axial layer orientation; exclude infarction; indication of encephalitis
|
|
T2w FLAIR
|
axial layer orientation; exclude SAH or demyelinating/inflammatory foci
|
|
T2w
|
sagittal layer orientation; evaluation of aqueduct, midbrain, cerebellum
|
|
T2*w (“hemo”)
|
assessment for microhemorrhage, older hemorrhage
|
|
arterial TOF angiography
|
assess brainstem arteries
|
|
arterial CE MRA
|
assess craniocerfical arteries; 0.1 mmol Gd/kg bodyweight; Care bolus technique, start
measurement when contrast agent is in aortic arch
|
|
Venous CE MRA (MRV)
|
assess veins and arteries
|
T1w = T1-weighted images; DWI = diffusion-weighted imaging; T2w = T2-weighted images;
T2*w = T2-weighted gradient echo images; CTA = arterial CT angiography; CTV – venous
CT venography; MRA = MR angiography; MRV = MR venography; CE = contrast enhanced
If there is suspicion of a vascular process, an arterial or venous CT angiography
can follow. An arterial angiography is performed after intravenous administration
of 60 ml of an iodine-based contrast agent with a concentration of 300 mg iodine/ml
with a flow rate of 6 ml/sec (64/128-slice MDCT) or 4 ml/sec (8/16-slice MDCT). The
scan direction is caudocranial; the examination uses semiautomatic bolus tracking
started at cervical vertebrae 5/6 if a threshold of 150 HE has been exceeded. In order
to simplify planning of potential endovascular therapy, the scan region should extend
from the aortic arch to the vertex. Venous CT angiography is performed in craniocaudal
scan direction after intravenous administration of 80 ml contrast media using a scan
delay of 45 sec with a 3 ml/sec flow rate. Using a shorter scan delay increases the
risk of insufficient contrast of the brain nerves.
If in the non-enhanced CT there is suspicion of an infectious or inflammatory event,
a contrast-enhanced examination should be performed 5 minutes after administration
of the contrast agent. It should be noted, however, that MRI is superior to CT as
verification of inflammatory changes.
MR-based diagnosis ([Table 2]) should be performed using a head coil. Care should be taken that examinations be
performed in at least two mutually orthogonal planes using two different weightings.
Using default 3 T, the authors acquire a T1-weighted (T1w) 3-D data record with a
1 mm isotropic resolution and secondary reconstruction on the axial and coronal plane.
Using 1.5 T MR systems, axial T1w images are acquired with a 4 mm slice thickness..
These are each followed by an axial T2-weighted (T2w) FLAIR sequence with a 3 mm slice
thickness. In this sequence particular attention is paid to the complete signal suppression
of the CSF. If this is lacking, it can be an indication of subarachnoid hemorrhage
or an inflammatory event. However, it should be noted that CSF signal suppression
might be due to additional pathological causes such as acute stroke, leptomeningeal
metastasis, administration of supplemental oxygen, or physiological processes such
as CSF pulsation [7]. In addition, images taken of all the patients include sagittal T2w images with
3 mm slice thickness to assess the midbrain and brain stem, axial T2*w sequences to
detect microhemorrhages as well as axial diffusion-weighted images with 5 mm slice
thickness and two diffusion factors (b = 0/1000 s/mm2).
If there is a related clinical suspicion of a vascular process, arterial angiography
employing the TOF (time-of-flight) technique can be used or performed as a contrast-enhanced
MR angiography (CE MRA). Routinely, representation of the intracranial vessels uses
TOF due to the higher spatial resolution than CE MRA for extracranial vessels [8]. As a rule, time-resolved CE MRA offers a diagnostic advantage only when there is
suspicion of intracranial arteriovenous malformation, and therefore has not been established
in clinical practice.
Likewise, various techniques are available for MR venography. Due to the brief required
examination time and low susceptibility to artifacts, contrast-enhanced MR angiography
is regularly performed in clinical practice. The procedure involves injection of 0.1 mmol
Gd per kg of bodyweight.
Depending upon the medical issue, the examination protocol can be modified just as
in CT imaging ([Table 3]).
Table 3
Special examination protocols for CT and MRI.
|
migraine
|
SAH
|
RCVS
|
pituitary apoplexy
|
dissection
|
sinus/venous thrombosis
|
intracranial cysts
|
infections
|
cerebral pseudotumors
|
CSF leak syndrome
|
trigeminal neuralgia
|
|
MRI
|
CT
|
CT
|
MRI
|
MRI
|
MRI
|
MRI
|
MRI
|
MRI
|
MRI
|
MRI
|
|
primary modality
|
primary modality
|
often primary modality for SAH
|
primary modality
|
primary modality
|
primary modality
|
standard program
|
primary modality for encephalitis
|
primary modality
|
primary modality
|
primary modality
|
|
standard protocol
|
non-enhanced CT
|
non-enhanced CT
|
standard protocol
|
standard protocol
|
standard program
|
sag. CISS to assess positional relationship of aqueduct, midbrain
|
standard program
|
ax T2w to assess ventricle, orbits, optic nerve pathway and bulbar configuration
|
head: ax T2w to assess possible hygroma
|
ax T2w to exclude demyelinating/inflammatory foci
|
|
for structural lesion T1w (5 min) post-contrast on at least 2 planes
|
arterial CTA
|
arterial CTA
|
cor T2w to distinguish optic chiasma
|
ax T1w to assess wall hematoma
|
CE-MRV
|
|
T1w post-contrast on at least 2 planes
|
cor T2w to assess optic nerve sheath
|
spine:
sag T2w fs to assess epidural fluid
cor T2w to assess meningeal diverticula
|
TOF MRA
ax CISS to detect neurovascular compression
|
|
|
|
T1w post-contrast cor and sag
|
CE MRA of craniocervical arteries
|
CT
|
CT
|
|
CE MRV to assess transverse sinus
|
|
|
|
CT
|
MRI
|
MRI
|
|
|
CCT
|
primarily for colloid cysts
|
CT
|
|
|
Tolosa-Hunt syndrome
|
|
only if CI for MRI, or MRI not available
|
if neg. CCT
|
primary modality for follow-up
|
CT
|
CT
|
CTV
|
|
primary modality to exclude CI prior to LP
|
|
|
MRI
|
|
+ TOF angiography
|
standard protocol
|
only if CI for MRI, or MRI not available
|
CCT
CTA
|
|
|
|
|
|
primary modality
|
|
|
+ TOF angiography
|
|
|
|
|
|
|
|
standard program
|
|
DSA
|
|
|
|
|
|
|
|
|
cor and ax T1w post-contrast to detect inflammatory lesions
|
|
If CTA ambiguous
for endovascular
therapy
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
CI = contraindications; LP = lumbar puncture; ax = axial layer orientation; cor = conronal
layer orientation; fs = fat-saturated imaging.
Intra-arterial angiography using DSA does not play a role in the primary diagnosis
of headache.
Secondary Headache
In a minority of cases, secondary headache is symptomatic of a different underlying
disorder. Following are descriptions of frequent symptom patterns and related changes
disclosed by imaging.
Subarachnoid Hemorrhage
Etiology
In 75 – 85 % of cases [15], non-traumatic SAH is related to a rupture of an aneurysm of vessels supplying the
brain. So-called perimesencephalic nonaneurysmal subarachnoid hemorrhage accounts
for 15 % of cases [15]; the cause of this is abnormal venous drainage into the subarachnoid space. In approx.
5 % of cases, SAH has a different cause, such as dissection of the intracranial vertebral
artery [16].
Symptomology
Thunderclap headache is the cardinal symptom in more than 75 % of patients Here, patients
with perimesencephalic SAH frequently exhibit a less fulminant onset of headache.
In addition, clinical symptoms can range from minor complaints to coma. Patients with
perimesencephalic SAH generally experience a more favorable clinical outcome.
Imaging
When there is clinical suspicion, the imaging method of choice ([Table 3]) is CCT with CTA [15]
[16]. In non-enhanced CCT, the subarachnoid space appears hyper-dense in cases of SAH,
whereas aneurysmal SAH is typically localized in the basal and ambient cisterns ([Fig. 1]). In comparison, perimesencephalic SAH is localized in the interpeduncular and prepontine
cisterns ([Fig. 1]) Since blood distribution is not pathognomic, a CTA must be performed in cases of
perimesencephalic SAH, however. The literature describes CT sensitivity for the detection
of SAH as 100 % within the first 6 hours after the event; after 24 hours, sensitivity
decreases to 93 %, and after 4 days, it declines to 50 % [17].
Fig. 1 a 28-year-old female patient with thunderclap headache with maximum pain within a few
minutes; plain CCT with identification of extensive subarachnoid hemorrhage (SAH)
in the basal cisterns. b Axial 10 mm MIP-reconstruction of the same patient revealed a saccular aneurysm of
the posterior communicating artery as the underlying cause of the hemorrhage. c 56-year old patient with thunderclap headache two days before admission and now dull
headache. Plain cranial CT without evidence of SAH. d CT angiography of the same patient demonstrates extensive vasospasm of the intracranial
vessels. CSF analysis was without evidence of SAH supporting the diagnosis of reversible
cerebral vasoconstriction syndrome.
FLAIR imaging during MRI is suitable for the detection of SAH. Subarachnoid blood
causes the intrathecal space to appear hyperintense in FLAIR [18].
In the primary diagnosis of SAH, CTA has replaced angiography using DSA, which as
a rule is only still employed in cases of ambiguous CTA findings or as part of endovascular
therapy [15]
[16].
If there is clinical suspicion of SAH, and in the absence of evidence of intracranial
blood in the CT or MRI, the suspected diagnosis must be excluded or confirmed via
lumbar puncture, since in such cases, spinal SAH must be considered [19].
Reversible Cerebral Vasoconstriction Syndrome
Etiology
Reversible cerebral vasoconstriction syndrome (RCVS) should be considered as part
of a differential diagnosis of patients with TCH and unremarkable CSF as well as indication
of segmented diameter variations of the intracranial vessels in the CT or MR angiography
([Fig. 1]). This is a heterogeneous group of disorders associated with reversible segmental
vasospasm of the intracranial vessels [20]. The primary differential diagnosis is the isolated angiitis of the CNS, where patients
with RCVS typically exhibit reversibility of the vascular changes within 4 weeks after
symptom onset [14]
[21].
Symptomology
Just as in cases of SAH, thunderclap headache is the leading symptom in 95 % of patients;
patients with RVCS frequently complain of recurring headaches.
Imaging
Due to the clinical symptom profile, patients with RVCS are frequently examined using
CCT or CTA. Unlike SAH, the basal cisterns are usually hypodense. Using CTA, narrow
vessels with significant diameter variations can be demonstrated ([Fig. 1]). With such symptoms, a differential diagnosis should also consider the possibility
of SAH with consecutive vasospasms no longer detectable in the CT, so that lumbar
puncture should be recommended [19].
Follow-up should entail MR imaging ([Table 3]), since in such cases diffusion-weighted images can reliably detect infarcts as
a possible complication [22]. Due to method-related higher sensitivity required to detect diameter variations,
imaging of the intracranial arteries should employ TOF angiography compared to contrast-enhanced
angiography (CE MRA) [23]. However, it should be considered that the resolution of MRA is less than that of
CTA.
The primary differential diagnosis is isolated angiitis of the CNS, which likewise
includes multiple stenosis of the intracranial vessels. However they are distally
and eccentrically localized in the arterial lumen, and after contrast is administered,
enhancement of the arterial wall can be observed. In addition, transient ischemia
and/or hemorrhages can frequently be detected [24]. Typically, patients with RVCS show reversibility of the vascular changes within
four weeks.
Pituitary Apoplexy
Etiology
Pituitary apoplexy is a rare but potentially life-threatening disorder which can be
caused by ischemic or hemorrhagic necrosis. Very frequently, affected patients have
a macroadenoma undergoing drug therapy or are taking oral anticoagulants; however,
in the majority of cases, no cause can be ascertained [25].
Symptomology
This involves a sudden headache accompanied by progressive vision loss [25].
Imaging
Neuroimaging should be promptly performed on patients when pituitary apoplexy is suspected
([Table 3]). MRI is the procedure of choice, whereby the pituitary signal is dependent upon
the time point of the examination after the event. Differentiation from optic chiasma
is best based upon T2w images. Contrast-enhanced images should be obtained in order
to differentiate non-infarcted tissue. However, evidence of hemorrhage can also be
obtained via CT ([Fig. 2]).
Fig. 2 Rare causes of secondary headache. a Plain axial cranial CT; 64-year old patient with known pituitary macroadenoma; TCH
and sudden loss of vision. The intra- and suprasellar adenoma (arrow) is hyperdense
indicating hemorrhagic pituitary apoplexy. b Contrast-enhanced axial T1-weighted sequence with fat suppression; 48-year-old female
patient with right sided orbital pain and paralysis of the third and fourth cranial
nerve. Strongly enhancing granulomatous tissue within the right cavernous sinus, superior
orbital fissure and dura of the middle cranial fossa (long arrow) and concomitant
narrowing of the right internal carotid artery (short arrow) as diagnostic landmark
of Tolosa-Hunt-Syndrome. c Plain axial cranial CT three weeks after a mild traumatic brain injury; 74-year-old
patient with oral anticoagulation treatment and two weeks history of headache. Subacute
subdural hematoma above both hemispheres; the cortical surface (arrow) is displaced
from the inner aspect of the cranium.
Dissection
Etiology
In a dissection there is a tear in the arterial wall and subsequent subintimal hemorrhage.
The result can be consecutive narrowing of the true lumen or formation of a pseudoaneurysm
if the tear is subadventitial [26]
[27]. In the majority of cases, dissection is spontaneous; additional risk factors include
trauma or manipulation of the cervical spine and pre-existing connective tissue disease
[26].
Symptomology
Headaches are the most common symptom of patients with dissection and as a rule they
appear prior to focal-neurological symptoms [26]. They occur more frequently during dissection of the internal carotid artery compared
to lesion of the vertebral artery ([Fig. 3]) Although headache generally exhibits gradual increase, up to 20 % of affected patients
present with TCH. Typically pain is unilateral on the same side as the affected vessel
and radiates from the neck into the head. In dissection of the vertebral artery, pain
is primarily localized occipitally; in carotid dissection, pain radiates into the
jaw, to the temple as well as around the eyes [26].
Fig. 3 a 27-year-old female patient with numb pain in the neck radiating into the temporal
region after physical exercises. CT angiography demonstrates circular mural hematoma
of the internal carotid artery (ICA). b Plain axial T1-weighted image with fat saturation of the same patient demonstrating
the hyperintense mural hematoma of the ICA (arrow). The hematoma can be very nicely
separated from the hypointense flow void causing discrete narrowing of the lumen.
c 37-year-old female patient with new onset of headache after playing with her toddler.
CT angiography demonstrates discrete luminal irregularities of the dominant left vertebral
artery within the horizontal part of atlas loop. d Plain axial T1-weighted image with fat saturation of the same patient demonstrates
the hyperintense mural hematoma indicating arterial dissection.
Imaging
MRI is the preferred imaging modality ([Table 3]). Non-enhanced T1-weighted images with fat saturation should be used to detect mural
hematoma as confirmation of dissection, since after the second or third day, the mural
hematoma appears hyperintense compared to the perfused lumen due to methemoglobin
formation [26]
[27]. In the acute phase, mural hematoma appears isointense. Vessel imaging can be performed
using either TOF MRA or CE MRA; the latter is preferred to display craniocervical
vessels [26]
[27]. As a rule, the arterial lumen tapers conically in a vascular occlusion caused by
dissection (so-called “string sign”).
Alternatively, CT angiography can be performed ([Fig. 3]). In this case, the intramural hematoma appears as localized wall thickening with
accompanying variations in diameter.
In clinical practice, Doppler ultrasound is successfully used as a screening examination
and for follow-up. However, ultrasound findings frequently require follow-up diagnostic
imaging, since only hemodynamic findings can be obtained and the etiology of the flow
obstruction observed via Doppler sonography remains unclear [27].
Cerebral Venous Sinus Thrombosis
Etiology
A number of risk factors exist for the formation of cerebral venous or sinus thrombosis
[28]. In particular, pregnant women and those in the postpartum phase have an increased
risk [29]. No causal factor can be identified in 20 – 25 % of cases.
Symptomology
The clinical symptom pattern is variable and can range from non-specific complaints
to focal-neurological deficits through to coma. The guiding symptom, however, is headache
[30]. Classically, headache has subacute onset and increases during gradual progression.
Imaging
Whereas in non-enhanced CCT, hyperdense interior veins have a high positive predictive
value as an indirect reference point for thrombosis [31], the value of the already hyperdense sinus in non-enhanced CCT is debatable ([Fig. 4]); this is also true of the lack of flow-related signal loss (so-called flow void
phenomenon) in T2-weighted images. In MRI, thrombus in the gradient echo appears as
tubular signal cancellation due to blood degradation products. Further, susceptibility-weighted
sequences, e. g. SWI (susceptibility-weighted imaging) or SWAN (susceptibility-weighted
angiography) should be suitable to definitively identify thrombosis of cortical veins
[32]. Nevertheless, vascular diagnosis should always follow in cases of doubt. In addition
to CT angiography, this can also be in the form of MR angiography; however, contrast-enhanced
MR venography ([Table 3]) is preferable to other techniques [32]. In both examination modalities, thrombus appears as a contrast defect ([Fig. 4]).
Fig. 4 a 27-year-old female patient 2 weeks postpartum. Slowly progressive headache which
is not responding to therapy. Plain cranial CT demonstrates hyperdense superior sagittal
sinus (arrow). b Sagittal MIP reconstruction (3 mm slice thickness) of a contrast-enhanced MR venography
of the same patient demonstrating extensive thrombosis of the superior sagittal sinus
(arrow).
Intracranial Cysts
Colloid cysts
Etiology
Colloid cysts are protein-rich cysts on the roof of the third ventricle ([Fig. 5]) emanating from the endoderm [33].
Fig. 5 a 23-year old patient with intermittent holocephalic headache. The colloid cyst in
typical location at the roof of the third ventricle (arrow) appears hyperdense on
plain cranial CT. b Coronal T2-weighted CISS sequence demonstrates the close anatomical relationship
of the colloid cyst (arrow) to both foramen of Monro (dotted arrow). The cyst appears
hypointense due the protein-rich content. c 25-year-old female fMRI volunteer subject with intermittent morning headache. Sagittal
T2-weighted CISS image demonstrates a large pineal gland cyst extending just in front
of the aqueduct.
Symptomology
Colloid cysts can be an incidental finding in cranial imaging or can manifest themselves
via headache. The cause can be assumed to be intermittent blockage of the interventricular
foramen. Since colloid cysts can exhibit rapid growth progression, they can result
in the formation of life-threatening obstructive hydrocephalus [33]. Therefore neurosurgical therapy should be suggested to patients with colloid cysts.
Imaging
In more than 90 % of cases, colloid cysts are found in the direct vicinity of the
interventricular foramen [33] and in non-enhanced CCT appear as hyperdense round lesions ([Table 3]). Cyst signal can be variable in an MRI, and depends on the viscosity and protein
makeup of the cyst contents[34]. As a rule they appear hypointense in T2w and hyperintense in T1w. Since they can
also appear to be CSF-isointense in an MRI, these cysts are frequently better distinguished
using CCT.
Pineal Cysts
Etiology
Pineal cysts are non-neoplastic cysts in the pineal canal.
Symptomology
Generally these are asymptomatic findings ([Fig. 5]) during imaging of the neurocranium, found in 2.5 – 10 % of all patients [33]. Because of this, some authors consider them only as a diagnosis of exclusion as
a cause of headache [35]. In addition to a disturbance of melanin metabolism, another possible cause under
discussion is intermittent compression of the tectal plate and aqueduct caused by
very large cysts. Infrequently very large cysts can result in compression of the tectal
plate accompanied by development of Parinaud’s Syndrome.
Since the majority of cysts are asymptomatic and consistent in size or can even exhibit
size reduction, follow-up is recommended; neurosurgical therapy is recommended only
for cysts > 10 – 14 mm [31].
Imaging
Imaging can employ either CT or MRI ([Table 3]); MRI should always be used for follow-up. In CT, the cyst is hypodense; in T1w
and T2w images it likewise indicates a hypointense signal. Cyst contents in FLAIR
images appear hyperintense. Sagittal high-resolution T2w sequences (e. g. using CISS)
should be acquired to accurately determine positional relationship of the cyst to
the tectum and aqueduct ([Fig. 5]).
Administration of contrast agent is not required for diagnosis. In up to 40 % of cases,
in both CT and MRI a linear marginal enrichment can be detected [33].
Intracranial infections
Etiology
In cases of cerebral infection, a distinction can be made between inflammation of
the cerebral parenchyma (encephalitis) and cerebral membranes (meningitis). In the
majority of cases, infections are either viral or bacterial in nature [36], and the path of infection is either hematogenic (e. g. during sepsis), through
neighboring tissue (as a result of otitis media or sinusitis), directly or iatrogenically.
Symptomology
The guiding symptom of intracranial infection is headache and fever. Depending on
the site and extent of the infection, additional neurological symptoms – including
death – may occur.
Particular attention, however, should be paid to immune system-compromised and HIV-positive
patients [37]. Intracranial pathology is found in cases of new-onset headache in up to 82 % of
these patients [38]
[39] ([Fig. 6]). Therefore, cerebral imaging should be performed after new-onset headache, or if
existing symptoms change in type or intensity.
Fig. 6 a 43-year-old patient with new onset of headache and fever. CSF analysis demonstrated
bacterial meningitis. Neurological worsening two days after onset of symptoms. Contrast-enhanced
CT demonstrates frontal epidural abscess (arrow) and subdural empyema (arrow heads).
b 29-year-old female patient with bacterial meningitis. Plain cranial CT in bone window
level setting demonstrates extensive frontal sinusitis as possible underlying cause.
c 37-year-old HIV-positive patient (T4 cell count < 200/µl) with new onset of headache.
Axial T2-weighted FLAIR image demonstrates left frontal cortical and subcortical lesion.
d Contrast-enhanced T1-weighted image of same patient demonstrates linear cortical
enhancement. Histologically- proven cerebral toxoplasmosis.
Imaging
Meningitis is a clinical diagnosis supported by testing cerebrospinal fluid. The use
of imaging, therefore, is to exclude contraindications for a lumbar puncture [40]. Performing non-enhanced CCT is sufficient here. In rare cases, moreover, complications
or entry points for an inflammatory process can be identified ([Fig. 6]).
If encephalitis is suspected, an MRI should be performed ([Table 3]). Inflammatory changes appear as hyperintense signal alterations in FLAIR images,
and in diffusion-weighted images can be distinguished earlier as hyperintense signal
alteration. Administration of contrast agent is required, and contrast-enhanced images
should be acquired on at least two planes.
Cerebral Pseudotumors
Etiology
CSF circulatory dysfunction can likewise be a source of headache. A particular form
of this is the cerebral pseudotumor, also characterized as idiopathic intracranial
hypertension [41]. This is understood to be an increase in intracranial pressure without evidence
of an intracranial mass, hydrocephalus or edema.
Symptomology
Typical symptoms are headache and loss of visual acuity. Additional common symptoms
include tinnitus as well as cranial nerve paresis; an ophthalmological examination
may reveal papilledema. Typically young, overweight women and older slender men are
affected, whereas among women, headache is in the forefront, and vision loss predominates
among men [41].
Imaging
MRI is the examination modality of choice. Typical imaging findings are flattening
of the papilla in axial T2w images as well as a gyrose optic nerve. Coronal images
reveal an enhancement of the optic nerve sheath; this phenomenon can be easily assessed
using T2w images with fat saturation ([Table 3]). Additionally, the pituitary is flattened (so-called empty sella syndrome). Venous
angiography frequently reveals stenosis in the transverse sinus [42]. Due to shorter examination time and reduced susceptibility to artifacts, contrast-enhanced
MR venography is preferable to TOF venography ([Table 2]). Morphological changes in the image can be reversed after lumbar puncture, a diagnostic
indicator ([Fig. 7])
Fig. 7 a 32-year-old obese female patient (BMI 32 kg/m2) with headache and progressive loss
of vision. Coronal T2-weighted sequence demonstrates dilated optical nerve sheaths
on both sides (arrow) as indirect sign of pseudotumor cerebri. b Sagittal T2-weighted image of the same patient demonstrates “empty sella”-phenomenon.
c Venous TOF angiography of the same patient delineating stenosis of the lateral transverse
sinus (arrow). d The stenosis of the transverse sinus is reversible (arrow) after spinal tap test
highly suggestive for the diagnosis pseudotumor cerebri.
CSF Leak Syndrome
Etiology
In contrast, the CSF leak syndrome is a relatively recent diagnosis that is underdetected.
The pathophysiological basis is that the loss of CSF results in caudal displacement
of the brain with subsequent strain on the richly innervated dura, causing headache
[43]. As it progresses, pain symptoms become chronic. A distinction can be made between
a primary idiopathic form and a secondary form. Causes of the secondary form can be
meningeal diverticula generally occurring along the nerve root, or dural defects.
The latter can be iatrogenic or caused by degenerative osteophytes. As many as 2/3
of patients additionally exhibit connective tissue disease.
Symptomology
The disease pattern is marked by orthostatic headache normally occurring after 15
minutes in the standing position and improving in the reclining position. Women are
more frequently affected than men, and peak age is about 40 [43]
Imaging
Diagnosis must be performed using MRI ([Table 3]) [43]. Intracranial subdural hygromas and sinus dilation are typically found, and after
administration of contrast agent, the meninges exhibit significant contrast accumulation
([Fig. 8]). Spinal epidural fluid deposits can be detected. These are easily detected in sagittal
T2-weighted images with fat saturation, since in these sequences, a distinction can
be reliably made between epidural fluid and fat. Coronal T2-weighted images are suitable
to identify nerve root sleeve cysts as a possible cause of CSF loss ([Fig. 8]) In up to 20 % of cases, the MRI is unremarkable, however. In addition to diagnosis,
radiology also offers the possibility of interventional radiological therapy using
an epidural blood patch [44].
Fig. 8 a 43-year-old female dancer with progressive headache in upright position. Axial T2-weighted
image demonstrates bilateral frontal hygroma (arrow). b Contrast enhanced coronal T1-weighted image of the same patient demonstrating thickened
and strongly enhanced meninges and tentorium. c Sagittal T2-weighted image with fat
suppression of the spine demonstrates epidural effusion (arrow) as indirect spinal
sign of intracranial hypotension. d Coronal T2-weighted MR-myelogram delineates multiple spinal nerve root diverticula
as possible cause of the CSF leakage. Complaints resolved after epidural blood patch
at the level of the largest diverticulum.
Sinusitis
Etiology
There are a number of triggering factors for sinusitis. With respect to their temporal
progression, a distinction can be made between an acute (less than 8 weeks duration
or fewer than 4 episodes per year) and a chronic form (more than 8 weeks duration
or more than 4 episodes per year) [45].
Symptomology
Sinus headaches as a rule generally have a dull character and mainly occur with involvement
of the sphenoid sinus ([Fig. 9]).
Fig. 9 a 33-year-old patient with new onset of holocephalic headache. Plain cranial CT in
bone window level setting demonstrating opacification of the left sphenoid sinus indicating
acute sinusitis. b 43-yearold patient with chronic sinusitis and recent exacerbation. Two-day history
of pain in the right eye and diplopia. Coronal CT reconstruction demonstrates a subperiostal
abscess at the roof of the orbit. c 47-year-old female patient with chronic sinusitis. Acute exacerbation with new onset
of headache and pain in the right eye. Coronal T2-weighted images demonstrate subtle
inflammatory changes around the optic nerve and extra- and intraconal fat tissue.
Imaging
Acute sinusitis is generally a clinical diagnosis and does not require imaging. However,
imaging should be performed in cases of chronic sinusitis to assess the anatomy with
respect to surgical therapy [46], in cases of immune system-deficient patients, new onset focal neurological deficit,
or if complications are suspected [45]
[47].
Due to their limited sensitivity and specificity, conventional X-ray images are obsolete
for the diagnosis of sinusitis; instead a low-dose CT should be performed [47]. Sinusitis is accompanied by swelling of the mucosa, which appears in CT as iso-
to hypodense; in MRI it appears hyperintense in T2w images, and isointense to the
musculature in T1w images. Chronic cases may result in sclerosis of the sinus walls
which is easily detectable in CT, and which can reduce the volume of the affected
sinus.
If there is suspicion of intracranial or orbital complications ([Fig. 9]), MRI is superior to CT as a diagnostic modality. These can be well-differentiated
in coronal T2-weighted images with fat saturation, as well as in fat-saturated T1-weighted
images after administration of contrast agent [47].
Trigeminal Neuralgia
Etiology
Trigeminal neuralgia (TN) is a neurovascular compression syndrome; according to the
IHS classification of headache, it belongs to the group of “cranial neuralgias, central
and primary facial pain and other headaches.” The cause is considered to be compression
of the nerve in its root entry zone by an artery [48], generally the superior cerebellar artery or the anterior inferior cerebellar artery
([Fig. 10]).
Fig. 10 a 57-year-old female patient with 7-month history of recurrent pain in the territory
of the second trigeminal branch. Axial T2-weighted CISS image demonstrates neurovascular
compression of the root entry zone of the left trigeminal nerve by a loop of the left
superior cerebellar artery. b Intraoperative photography of the same patient. The nerve (o) is flattened (arrow)
by the pulsatile compression of the vascular loop (x). c 24-year-old female patient with 2-week history pain in the territory of the first
trigeminal branch. Axial T2-weighted image demonstrates demyelinating lesion at the
root exit zone. d Coronal reconstructed contrast-enhanced T1-weighted MPR image demonstrates enhancement
of the lesion indicating active inflammation.
Symptomology
Typically patients complain of intense pain lasting but a few seconds in the region
of the second or third trigeminal branch; in only 5 % of cases is the pain in the
territory of the ophthalmic nerve (first branch). Pain can occur spontaneously or
can be provoked by contact with trigger points [48].
Imaging
If TN is suspected, diagnosis should be performed using MRI ([Table 3]). The success of surgical therapy correlates with the preoperative verification
of neurovascular compression. The examination protocol to substantiate this should
include axial high-resolution T2-weighted images (e. g. CISS sequence) in addition
to arterial TOF angiography. It should be noted, however, that among healthy subjects,
vessel-nerve contact can likewise be observed; therefore there must always be a correlation
between image findings and clinical symptoms [48]. A differential diagnosis of multiple sclerosis should be considered, particularly
in cases of young women with new-onset TN or new-onset atypical facial pain ([Fig. 10]).
Tolosa-Hunt Syndrome
Etiology
Together with trigeminal neuralgia, Tolosa-Hunt syndrome (THS) is counted among the
group of cranial neuralgias. The disorder is characterized by inflammatory granulomatous
changes of unknown etiology in the cavernous sinus and superior orbital fissure which
can extend into the orbit and continue intracranially [49].
Symptomology
THS is an episodically recurring pain in the orbit, accompanied by paresis of the
oculomotor nerve and trochlear nerve and/or the abducens nerve [49].
Imaging
MRI is the modality of choice. In addition to prompt improvement of symptoms within
72 hours after administration of cortisone, detection of inflammatory changes ([Fig. 2]) is one of the essential diagnostic criteria [49]. To demonstrate granulomatous changes, contrast-enhanced images with fat saturation
should be acquired using axial and coronal layer orientation ([Table 3]).
Post-traumatic Headache
Etiology
Headache is one of the most common symptoms after traumatic brain injury (TBI), and
the most frequent form of secondary headache [4]
[50]. The exact pathophysiological mechanism is not understood in the majority of cases.
Paradoxically, mild TBI is more frequently associated with chronic post-traumatic
headache than severe TBI [50].
Symptomology
According to guidelines, post-traumatic headache appears within seven days after the
trauma and is considered acute if it lasts less than 3 months [4]. Post-traumatic headache does not exhibit specific characteristics, and current
studies have shown that in the majority of cases, post-traumatic headaches have a
migrainoid character [50]. In addition they can be associated with impairment of cognitive function, leading
to a significant reduction in the quality of life.
Imaging
In rare cases there is a correlation in morphological imaging [50]; therefore, initial imaging can use non-enhanced CCT. In the differential diagnosis,
a subdural hematoma should be considered, particular in older patients undergoing
anticoagulant therapy ([Fig. 2]). CCT is the imaging modality of choice. Hematoma appears hyperdense compared to
the adjoining cerebral parenchyma. However, with progression it reduces in density,
so that the hematoma can appear isodense or hypodense with respect to the brain. Therefore
it is important to note whether the cortical relief touches the calvaria, which is
otherwise an indication of subdural hematoma.
