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Post partum neurological complications: Looking beyond PRES and CVT- A Pictorial review

Authors:
  • Columbia Asia referral Hospital, Yeshwantpur,
  • Manipal Hospital Yeshwantpur, Bangalore
Page 1 of 44
Post partum neurological complications: Looking beyond
PRES and CVT- A Pictorial review
Award: Magna Cum Laude
Poster No.: C-1365
Congress: ECR 2017
Type: Educational Exhibit
Authors: H. C. Chadaga1, S. Patwari1, A. Rohatgi1, M. Kumar1, A. Nagadi2;
1Bangalore/IN, 2Southampton/UK
Keywords: CNS, Neuroradiology brain, MR, CT, Complications, Obstetrics
DOI: 10.1594/ecr2017/C-1365
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Page 2 of 44
Learning objectives
The purpose of this educational exhibit is to:
To enumerate various neurological complications that occurs in postpartum
state.
To illustrate the imaging spectrum and MRI features of postpartum
neurological complications.
Background
Women during pregnancy and postpartum state undergo various physiological,
hemodynamic and hormonal changes which are essential to sustain the normal
pregnancy. There has been an increase in overall average age of pregnancy with
concomitant increased incidence of gestational hypertension and diabetes mellitus [1].
Neurologic signs and symptoms in pregnant and postpartum women may be due
to the exacerbation of a pre-existing medical condition, the initial manifestation of a
primary central nervous system-related problem, or a neurologic problem unique to
pregnancy and the postpartum period [2] the most common being posterior reversible
encephalopathy syndrome (PRES) and cerebral venous thrombosis (CVT). However
with increasing incidence of post partum complications, the radiologist needs to be
aware of various other cerebrovascular, neuroendocrine and metabolic complications
that manifest during this period.
Page 3 of 44
Fig. 1: POSTPARTUM NEUROLOGICAL COMPLICATIONS
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
Images for this section:
Fig. 1: POSTPARTUM NEUROLOGICAL COMPLICATIONS
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 4 of 44
Findings and procedure details
A pictorial review of pathophysiology and imaging of PRES and CVT are
described. We also review other cerebrovasclar complications like ischemic stroke
and hypertensive gangliocapsular hemorrhage, aneurysmal and non-aneurysmal
subarachnoid hemorrhage and postpartum cerebral angiopathy. We have also described
uncommon metabolic conditions in postpartum state like Wernicke's encephalopathy
and hypernatremic osmotic cerebral demyelination which can sometimes be confused
with PRES. Pituitary pathologies which are characteristically seen in postpartum state
like Pituitary apoplexy/Sheehan's syndrome and lymphocystic hypophysitis are also
described.
POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME (PRES) - ECLAMPTIC
ENCEPHALOPATHY:
PRES is one of the complications of preeclampsia, eclampsia, and
pregnancy-induced severe hypertension. The constellations of symptoms
are caused by reversible ischemia most commonly of the posterior cerebral
vasculature.
The predilection for the posterior circulation and watershed zones is
believed to be related to its sparse vasomotor sympathetic innervations.
The term PRES can be a misnomer as the syndrome can involve anterior
circulation territories. Furthermore, most cases involve a resolution of
changes with the treatment of the precipitating cause and clinical recovery
some patients can progress to develop permanent cerebral injury and be left
with residual neurological defects.
Patients typically experience a combination of headache, altered mentation,
visual disturbance, severe hypertension, and generalized seizures.
MR images show the typical symmetric edema in the parietal and occipital
lobes at the gray matter-white matter junctions. Similar changes may also be
seen in the frontal lobes, inferior temporo-occipital junction, and cerebellum.
In addition, patchy areas of vasogenic edema may be seen in the basal
ganglia, brainstem, and deep white matter. These changes are mainly due
to vasogenic edema and are reversible. In more severe cases, there may be
associated cytotoxic edema due to infarction. Rarely, tiny hemorrhages are
seen on susceptibility-weighted MR images.
Page 5 of 44
Fig. 2: MECHANISM OF PRES
References: http://www.thelancet.com/cms/attachment/2035219942/2050610577/
gr1_lrg.jpg
Page 6 of 44
Fig. 3: PRES in a 32-year old postpartum woman. Axial fluid-attenuated inversion-
recover MR images show typical symmetric, hyperintense vasogenic edema in the
parietal, occipital, and frontal lobes bilaterally at the gray matter-white matter junctions
with patchy areas of involvement of bilateral basal ganglia.
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
Page 7 of 44
Fig. 4: PRES in a 32-year old postpartum woman. Diffusion weighted MR images
show patchy areas of diffusion restriction in bilateral cerebral hemispheres at the gray
matter-white matter junctions and bilateral basal ganglia.
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
Page 8 of 44
Fig. 5: PRES in a 32-year old postpartum woman. Follow up imaging after 1 month
Axial fluid-attenuated inversion-recover MR images show significant resolution of
previously seen FLAIR changes.
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
CEREBRAL VENOUS SINUS THROMBOSIS:
The highest incidence of cerebral venous thrombosis is during first 2 weeks
of puerperium [3]. It accounts for 6% of maternal deaths; thus, a prompt
diagnosis and initiation of therapy is essential
The clinical presentation varies from headache to coma, depending largely
on the severity and extent of thrombosis as well as the mode of onset.
Page 9 of 44
Nonenhanced CT, which is less sensitive than MR imaging, may reveal
focal or diffuse high-attenuating venous sinuses, areas of cerebral edema,
and/or parenchymal hemorrhage. The sensitivity of CT can be enhanced
further by the intravenous administration of iodinated contrast material or
CT venography; both will reveal focal venous cutoffs or filling defects in the
sinus, with peripheral enhancement-that is, the "empty-delta" sign. [2]
MRI can show areas of parenchymal edema / infarcts or parenchyma
hemorrhages particularly at grey-white junction. An adjacent T1/ FLAIR
hyperintense vein with blooming on SWI / loss of normal flow void in
adjacent dural sinus can help to promptly plan MRV which can show
non-visualization of dural sinuses. Sometimes Contrast MRV need to be
performed particularly in cases of cortical vein thrombosis to show the filling
defects.
Anticoagulation therapy remains the first line of treatment, with thrombolysis
as an alternative treatment option-especially in patients with hemorrhagic
infarcts
Page 10 of 44
Fig. 6: 29-year-old woman with CVT who presented with a severe
headache and seizure 4 days after giving birth. Diffusion weighted MR
image shows asymmetrical areas of diffusion restriction in bilateral frontal
lobes
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia
Referral Hospital-Yeshwanthpur - Bangalore/IN
Fig. 7: 29-year-old woman with CVT who presented with a severe
headache and seizure 4 days after giving birth. Axial gradient-echo MR
image shows areas of blooming along superior sagittal sinus and cortical
veins (Star) with small foci of parenchymal blooming in right frontal lobe
(arrow)
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia
Referral Hospital-Yeshwanthpur - Bangalore/IN
Page 11 of 44
Fig. 8: 29-year-old woman with CVT who presented with a severe
headache and seizure 4 days after giving birth. Phase Contrast MR
venogram image shows non-visualisation of superior sagittal sinus
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia
Referral Hospital-Yeshwanthpur - Bangalore/IN
ACUTE ISCHEMIC STROKE/ PARENCHYMAL HEMORRHAGE:
Pregnancy and the puerperium are considered hypercoagulable states.
Factors leading to hypercoagulability of blood include low levels of inhibitors
of the coagulant protein S; elevated levels of inhibitors of protein C;
increased levels of fibrinogen, factor VII, factor VIII, and factor X; and an
enhanced ability to neutralize heparin [4]
Accelerated hypertension in eclampsia can cause intraparenchymal
hemorrhage.
The risk of both ischemic infarction, which accounts for 60% of all
strokes, and intracranial hemorrhage is high in the peripartum period and
puerperium, but not during the 9-month course of pregnancy itself.
Page 12 of 44
The clinical manifestations and imaging features are similar to those
associated with acute thrombotic and embolic strokes and hemorrhage in
non pregnant patients
Fig. 9: Acute arterial stroke in 33-year-old woman with H/O LSCS 10 days back
presenting to ER with acute left-sided weakness. Diffusion weighted MR image reveal
diffusion restriction in MCA territory (arrows) with occlusion at M1 segment of right
MCA on 3D TOF MR angiography (arrow).
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
SUBARACHNOID HEMORRHAGE
Subarachnoid hemorrhage (SAH) is a rare occurrence during pregnancy
and puerperium with rupture of an intracranial aneurysm still remains the
commonest cause of SAH. Pregnancy may increase the risk of aneurysm
rupture due to the hemodynamic and hormonal alterations. [4]
Primary nonaneurysmal SAH due to pregnancy-induced hypertension is an
extremely rare event. If seen, it is unilateral minimal SAH over the frontal or
parietal convexities. Unlike patients with aneurysmal rupture, hemorrhage
within the basal cisterns or ventricles is never seen. Shah [5] hypothesized
that SAH is possibly related to sudden hypertension and failure of cerebral
Page 13 of 44
autoregulation with propagation of the high arterial pressure waves to the
relatively thin-walled pial veins, resulting in their rupture.
Fig. 10: Nonaneurysmal SAH in a 35-year old postpartum woman who presented with
severe headache and hypertension. Axial head CT image shows a high attenuating
area (arrow), suggestive of SAH over left temporoparietal convexity sulci. Axial fluid-
attenuated inversion- recovery MR image shows a hyperintense area (arrow) in the
sulci consistent with SAH
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
Page 14 of 44
Fig. 11: Nonaneurysmal SAH in a 35-year old postpartum woman who presented with
severe headache. CT angiographic findings were normal.
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
POSTPARTUM CEREBRAL ANGIOPATHY:
Postpartum cerebral angiopathy (PCA) is a unique and poorly understood
cerebrovascular disease that occurs in normotensive postpartum women
within 1-4 weeks of delivery
There are two recognizable forms of PCA described in the literature.
Page 15 of 44
Idiopathic PCA (Call-Fleming postpartum angiopathy ) is a reversible
nonrelapsing angiopathy that occurs in normotensive postpartum women
who present with severe headache, seizures, and focal neurologic deficits
due to intracerebral hemorrhage
Iatrogenic PCA occurs anytime during the puerperium after administration
of bromocriptine to suppress lactation, administration of ergot alkaloids
to control postpartum hemorrhage, or use of sympathomimetics in cold
medicines and nasal decongestants.
Conventional MRI may be normal or sometimes show areas of cortical
edema or parenchymal hemorrhage
The angiographic features are characterized by reversible multifocal
stenoses and a beaded appearance of the medium- and small-caliber
cerebral arteries in the anterior circulation.
This is in contradiction to eclampsia, which affects large and medium-sized
arteries in the posterior circulation
Page 16 of 44
Fig. 12: Presumed Postpartum Cerebral Angiopathy in a 33 year old normotensive
lady with seizures and headache on postpartum 4th day. (A,B) Axial fluid attenuated
inversion recovery and susceptibility weighted MR images show right frontal lobar
haemorrhage (arrow) with sulcal FLAIR hyperintensity and blooming on SWI
suggestive of SAH (star). Also seen is right parietal cortical/subcortal edema (circle)
(C,D) Axial fluid attenuated inversion recovery and susceptibility weighted MR images
show focus of haemorrhage in left lentiform nucleus. MRA and MRV (not shown) were
normal
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
Page 17 of 44
PITUITARY APOPLEXY
Acute hemorrhagic infarction of either the physiologically enlarged pituitary
gland or an existing pituitary adenoma
As the gland suddenly enlarges it may cause compression of structures
adjacent to the sella, and thus lead to a number of signs and symptoms,
including sudden headache loss of visual acuity with a chiasmal field defect
and oculomotor palsies. In addition, the patient may experience decreased
level of consciousness, hypopituitanism and Addisonian crisis
The diagnosis of pituitary apoplexy is based on high clinical suspicion and
pituitary CT or MR imaging findings.
CT images may show a pituitary mass with a hyperdense hemorrhage in the
acute setting.
MR images may show a hemorrhagic pituitary mass with sometimes fluid
levels and an associated mass effect on surrounding structures. Signal
intensity changes on T1- and T2-weighted MR images are based on the
stage of hemorrhage.
Fig. 13: Pituitary apoplexy follow up MR imaging in a 33 years old lady with prior
history of severe postpartum headache and loss of visual acuity. Sagittal and Coronal
Page 18 of 44
T1 weighted MR image shows partial empty sella with thin T1 hyperintense pituitary
(arrow) suggestive of prior bleed.
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
SHEEHAN'S SYNDROME
Panhypopituitarism that results from acute ischemic pituitary gland necrosis
that is caused by severe postpartum hemorrhage and shock.
The diagnosis of Sheehan syndrome is based on the combination of
pituitary-related hormone assay and MR imaging findings.
During the acute phase of Sheehan syndrome, there is nonhemorrhagic
enlargement of the hypophysis with central hypointensity on T1-weighted
MR images, hyperintensity on T2-weighted MR images and peripheral
enhancement on postcontrast MR images.
Within several weeks to months, the pituitary gland will have severe atrophy,
leading to the appearance of an empty sella on MR images.
LYPHOCYTIC HYPOPHYSITIS:
Rare chronic inflammatory disorder of the pituitary gland and stalk, seen
most frequently in women (strong female predilection with a F:M of ~ 9:1)
and often in the postpartum period or the third trimester of pregnancy.
It is believed to be an autoimmune disease, with humoral and cell-
mediated components, that results in the destruction of the pituitary gland.
Histopathologic examination reveals lymphocyte and plasma cell infiltration
infiltration of the gland, parenchymal destruction, and fibrosis
Clinical presentation is varied depends on the part of the pituitary affected and
the size of the lesion. Lymphocytic hypophysitis can thus be classified as:
Anterior pituitary: lymphocytic adenohypophysitis (LAH)--most common
type, presents with endocrine hormone deficits and/ or mass effects on
adjacent structures (e.g. optic chiasm)
Posterior pituitary: lymphocytic infundibular neurohypophysitis (LINH)--
rare and presents with diabetes insipidus
Both anterior and posterior pituitary: lymphocytic infudibular panhypophysitis
(LIPH)
MR images show loss of normal posterior pituitary bright spot with
enlargement of the pituitary gland and homogenous / heterogenous post
contrast enhancement. There is infundibular thickening with occasional
adjacent dural / sphenoid sinus mucosal enhancement.
Parasellar T2 hypointense sign can be useful to in differentiating lymphocytic
hypophysitis from a pituitary adenoma
Page 19 of 44
Fig. 14: Lymphocytic adenohypophysitis in a 30-year-old postpartum woman who
presented with severe headache. Sagittal nonenhanced T1-weighted MR image
shows diffuse enlargement of the adenohypophysis with loss of normal posterior
pituitary bright spot (arrow). Sagittal GD-enhanced T1-weighted MR image shows
heterogeneous enhancement of the pituitary gland (arrow) and infundibulum (arrow).
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
Page 20 of 44
Fig. 15: Lymphocytic infundibuloneurohypophysitis in a 26-year-old postpartum
woman who presented with diabetes insipidus. Sagittal nonenhanced T1-weighted
MR image shows loss of normal posterior pituitary bright spot (arrow). Sagittal GD-
enhanced T1-weighted MR image shows enhancement of the thickened infundibulum
(arrow).
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
WERNICKE ENCEPHALOPATHY:
Wernicke encephalopathy is an acute severe neuropsychiatric syndrome
that results from thiamine deficiency
The characteristic presentation includes nystagmus and ophthalmoplegia,
mental status changes, and unsteadiness of stance and gait, which is seen
in a minority of these patients.
The majority of pregnant/ postpartum patients with Wernicke
encephalopathy present with nonspecific symptoms such as dizziness,
headache, fatigue, and depressive or visual problems.
MR imaging of the brain will reveal T2 hyperintense areas with/without
diffusion restriction in the dorspmedial thalami, mammillary bodies,
periaqueductal gray substance and periventricular gray matter surrounding
the third ventricle
Page 21 of 44
Fig. 16: Wernicke encephalopathy in a 29-year-old woman who had severe
hyperemesis gravidarum throughout pregnancy. Axial fluid-attenuated inversion-
recovery and Diffusion weighted MR image shows bilateral symmetrical FLAIR
hyperintensity with some diffusion restriction in dorsomedial thalami, mammillary
bodies and periaqueductal grey (arrows)
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
POSTPARTUM HYPERNATREMIC OSMOTIC DEMYELINATION
Osmotic demyelination syndrome resulting from postpartum hypernatremia
is a recently described entity wherein young women present with
hypernatremic encephalopathy and white matter hyperintensities. It is an
acute monophasic condition with acute hypernatremia occurring during
puerperium with good recovery in majority of the patients with treatment [6]
Page 22 of 44
MRI shows T2/DWI hyperintensities of corpus callosum, especially the
splenium with variable involvement of internal capsule, cerebellar peduncles,
pons, and hippocampus.
There can be symmetrical hyperintensity of the white matter in corticospinal
tracts from internal capsule to pons producing 'wine glass' appearance.
Fig. 17: Recurrent postpartum hypernatremic osmotic demyelination in a 29 years
old postpartum lady who presented to ER with altered sensorium and elevated serum
sodium. Axial diffusion weighted MR image shows symmetrical diffusion restriction
along bilateral posterior limbs of internal capsule extending into cerebral peduncles
with diffusion restriction in posterior body and splenium of corpus callosum (arrows).
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
Page 23 of 44
Fig. 18: Recurrent postpartum hypernatremic osmotic demyelination in a 29 years
old postpartum lady who presented to ER with altered sensorium and elevated serum
sodium. Coronal T2 weighted MR image shows symmetrical hyperintensity along
bilateral posterior limbs of internal capsule (arrows) extending into cerebral peduncles
resembling wine glass appearance. There is hyperintensity seen in posterior body and
splenium of corpus callosum.
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
Page 24 of 44
INTRACRANIAL HYPOTENSION:
With the more frequent use of spinal anesthesia and epidural analgesia
during pregnancy and delivery, intracranial hypotension is not an uncommon
complication and is seen especially during the postpartum period
Brain MR images show diffuse dural thickening and enhancement,
enlargement of dural sinuses, sagging of the brain, low-lying cerebellar
tonsils and subdural collections
Contrast-enhanced spine MR images may show thickening of the spinal
dura, extraarachnoidal fluid collections, and epidural venous dilatations.
Occasionally, sagittal T2-weighted MR images or MR myelograms show
cerebrospinal fluid leakage if the leak is active or cerebrospinal fluid
collection if the leak is not active.
The first line treatment is conservative and involves bed rest to decrease the
pressure and facilitate dural healing. When this measure is unsuccessful, a
dural blood patch procedure can be performed.
Page 25 of 44
Fig. 19: Intracranial hypotension in a 24 year-old postpartum woman in whom epidural
analgesia was induced during delivery. (A)(B) Axial and coronal T2-weighted MR
image shows bilateral subdural collections (arrows). (C) Axial post GD T1-weighted MR
image shows diffuse dural enhancement (arrows). (D) Sagittal non contrast T1 image
shows venous distension sign (curved arrow) with inferior convexity of dominant right
transverse sinus.
References: RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral
Hospital-Yeshwanthpur - Bangalore/IN
PREEXISTING CONDITIONS / INITIAL MANIFESTATION OF PRIMARY CNS
ILLNESS
The incidence and imaging of infective / neoplastic conditions are same as
nonpregnant states.
Page 26 of 44
Neurocysticercosis (NCC) is the major cause of adult-onset epilepsy in the
developing world and is caused by infection of the central nervous system.
Due to the paucity of reported cases, it is uncertain if pregnancy/ puerperium
is associated with an increased risk of reactivation of NCC.
The effect of pregnancy on multiple sclerosis has been a subject of debate
for many years. It is proposed that the varied effects of the hormones
secreted during pregnancy may induce an immunosuppressive effect. The
rate of multiple sclerosis relapse decreases during pregnancy, especially
during the third trimester. However, it has also been reported that there is a
return to the standard risk of relapse, or even rebound relapse, during the
postpartum period. [2]
The results of more recent studies have shown that nonruptured AVMs are
not associated with an increased risk of rupture during pregnancy [8]. There
is, however, a higher risk for repeat AVM rupture during pregnancy owing to
the hemodynamic changes that occur.
Images for this section:
Fig. 2: MECHANISM OF PRES
© http://www.thelancet.com/cms/attachment/2035219942/2050610577/gr1_lrg.jpg
Page 27 of 44
Fig. 3: PRES in a 32-year old postpartum woman. Axial fluid-attenuated inversion-
recover MR images show typical symmetric, hyperintense vasogenic edema in the
parietal, occipital, and frontal lobes bilaterally at the gray matter-white matter junctions
with patchy areas of involvement of bilateral basal ganglia.
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 28 of 44
Fig. 4: PRES in a 32-year old postpartum woman. Diffusion weighted MR images show
patchy areas of diffusion restriction in bilateral cerebral hemispheres at the gray matter-
white matter junctions and bilateral basal ganglia.
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 29 of 44
Fig. 5: PRES in a 32-year old postpartum woman. Follow up imaging after 1 month Axial
fluid-attenuated inversion-recover MR images show significant resolution of previously
seen FLAIR changes.
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 30 of 44
Fig. 6: 29-year-old woman with CVT who presented with a severe headache and seizure
4 days after giving birth. Diffusion weighted MR image shows asymmetrical areas of
diffusion restriction in bilateral frontal lobes
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 31 of 44
Fig. 7: 29-year-old woman with CVT who presented with a severe headache and seizure
4 days after giving birth. Axial gradient-echo MR image shows areas of blooming along
superior sagittal sinus and cortical veins (Star) with small foci of parenchymal blooming
in right frontal lobe (arrow)
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 32 of 44
Fig. 8: 29-year-old woman with CVT who presented with a severe headache and seizure
4 days after giving birth. Phase Contrast MR venogram image shows non-visualisation
of superior sagittal sinus
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 33 of 44
Fig. 9: Acute arterial stroke in 33-year-old woman with H/O LSCS 10 days back
presenting to ER with acute left-sided weakness. Diffusion weighted MR image reveal
diffusion restriction in MCA territory (arrows) with occlusion at M1 segment of right MCA
on 3D TOF MR angiography (arrow).
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 34 of 44
Fig. 10: Nonaneurysmal SAH in a 35-year old postpartum woman who presented with
severe headache and hypertension. Axial head CT image shows a high attenuating
area (arrow), suggestive of SAH over left temporoparietal convexity sulci. Axial fluid-
attenuated inversion- recovery MR image shows a hyperintense area (arrow) in the sulci
consistent with SAH
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 35 of 44
Fig. 11: Nonaneurysmal SAH in a 35-year old postpartum woman who presented with
severe headache. CT angiographic findings were normal.
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 36 of 44
Fig. 12: Presumed Postpartum Cerebral Angiopathy in a 33 year old normotensive lady
with seizures and headache on postpartum 4th day. (A,B) Axial fluid attenuated inversion
recovery and susceptibility weighted MR images show right frontal lobar haemorrhage
(arrow) with sulcal FLAIR hyperintensity and blooming on SWI suggestive of SAH (star).
Also seen is right parietal cortical/subcortal edema (circle) (C,D) Axial fluid attenuated
inversion recovery and susceptibility weighted MR images show focus of haemorrhage
in left lentiform nucleus. MRA and MRV (not shown) were normal
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 37 of 44
Fig. 13: Pituitary apoplexy follow up MR imaging in a 33 years old lady with prior history of
severe postpartum headache and loss of visual acuity. Sagittal and Coronal T1 weighted
MR image shows partial empty sella with thin T1 hyperintense pituitary (arrow) suggestive
of prior bleed.
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 38 of 44
Fig. 14: Lymphocytic adenohypophysitis in a 30-year-old postpartum woman who
presented with severe headache. Sagittal nonenhanced T1-weighted MR image shows
diffuse enlargement of the adenohypophysis with loss of normal posterior pituitary
bright spot (arrow). Sagittal GD-enhanced T1-weighted MR image shows heterogeneous
enhancement of the pituitary gland (arrow) and infundibulum (arrow).
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 39 of 44
Fig. 15: Lymphocytic infundibuloneurohypophysitis in a 26-year-old postpartum woman
who presented with diabetes insipidus. Sagittal nonenhanced T1-weighted MR image
shows loss of normal posterior pituitary bright spot (arrow). Sagittal GD-enhanced T1-
weighted MR image shows enhancement of the thickened infundibulum (arrow).
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 40 of 44
Fig. 16: Wernicke encephalopathy in a 29-year-old woman who had severe hyperemesis
gravidarum throughout pregnancy. Axial fluid-attenuated inversion-recovery and
Diffusion weighted MR image shows bilateral symmetrical FLAIR hyperintensity with
some diffusion restriction in dorsomedial thalami, mammillary bodies and periaqueductal
grey (arrows)
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 41 of 44
Fig. 17: Recurrent postpartum hypernatremic osmotic demyelination in a 29 years old
postpartum lady who presented to ER with altered sensorium and elevated serum
sodium. Axial diffusion weighted MR image shows symmetrical diffusion restriction
along bilateral posterior limbs of internal capsule extending into cerebral peduncles with
diffusion restriction in posterior body and splenium of corpus callosum (arrows).
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 42 of 44
Fig. 18: Recurrent postpartum hypernatremic osmotic demyelination in a 29 years old
postpartum lady who presented to ER with altered sensorium and elevated serum
sodium. Coronal T2 weighted MR image shows symmetrical hyperintensity along bilateral
posterior limbs of internal capsule (arrows) extending into cerebral peduncles resembling
wine glass appearance. There is hyperintensity seen in posterior body and splenium of
corpus callosum.
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 43 of 44
Fig. 19: Intracranial hypotension in a 24 year-old postpartum woman in whom epidural
analgesia was induced during delivery. (A)(B) Axial and coronal T2-weighted MR image
shows bilateral subdural collections (arrows). (C) Axial post GD T1-weighted MR image
shows diffuse dural enhancement (arrows). (D) Sagittal non contrast T1 image shows
venous distension sign (curved arrow) with inferior convexity of dominant right transverse
sinus.
© RADIOLOGY, Columbia Asia Referral Hospital, Columbia Asia Referral Hospital-
Yeshwanthpur - Bangalore/IN
Page 44 of 44
Conclusion
CONCLUSION:
It is important to make the distinction between the benign and more serious
neurologic signs, symptoms and complications seen in postpartum women.
Since many of these signs and symptoms overlap, this distinction may be
challenging for the clinician.
A varied spectrum of imaging findings may be encountered in the post
partum state. Knowledge of the various pathological processes and their
distinctive imaging findings is important in early diagnosis and management.
Personal information
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ResearchGate has not been able to resolve any citations for this publication.
Article
A number of physiologic, hormonal, immunologic, and hemodynamic changes take place in the maternal body during pregnancy. The majority of these changes are essential for maintaining the normal course of pregnancy. However, these changes may also cause acute or chronic conditions that affect various biologic systems in the mother. In addition, conditions of the central and peripheral nervous systems can cause a variety of neurologic symptoms and complications. Neurologic signs and symptoms in pregnant and postpartum women may be due to the exacerbation of a preexisting medical condition, the initial manifestation of a primary central nervous system–related problem, or a neurologic problem unique to pregnancy and the postpartum period. Because the symptoms of these conditions are either nonspecific or overlapping, it can be challenging to pinpoint the diagnosis clinically. These conditions can be classified into more commonly seen conditions such as headache, venous thrombosis, preeclampsia, subarachnoid hemorrhage, posterior reversible encephalopathy syndrome, and certain pituitary disorders; and less commonly seen entities such as aneurysm, arteriovenous malformation, primary or secondary neoplasm, Sheehan syndrome, and Wernicke encephalopathy. Imaging has an important role in the differentiation and exclusion of various neurologic conditions, and most of the time, imaging findings can point the clinician to a specific diagnosis. The imaging appearances of common and uncommon neurologic conditions that can occur during pregnancy and the early postpartum period are highlighted in this article.
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Article
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