MRI of Fetal and Maternal Diseases in Pregnancy 1st ed.

15. MR of Maternal Brain Diseases in Pregnancy

Alberto Pierallini  and Andrea Romano2, 3


Department of Radiology, IRCCS San Raffaele, Pisana, Rome, Italy


Department of Neuroradiology, IRCCS San Raffaele, Pisana, Rome, Italy


Azienza Ospedaliera S.Andrea, Università Sapienza, Rome, Italy

Alberto Pierallini


Acute neurological symptoms in pregnant and postpartum women could be caused by worsening of preexisting neurological conditions (multiple sclerosis or a seizure disorders) or by an initial presentation of a nonpregnancy-related problem (brain neoplasm). Patients can present with new acute-onset neurological conditions that are common during or after pregnancy. Knowledge of these conditions associated with pregnancy allows recognizing characteristic imaging finding to reach the correct diagnosis.

15.1 Clinical Presentations

15.1.1 Headache-Acute Neurological Deficit-Seizures

Primary headache disorders are the most common causes of headache in both pregnant and postpartum women. Usually, migraine improves during pregnancy due to the increased of estrogen levels. When pregnant patients get new, worsening headaches or when headaches change in character, secondary causes might exist [1].

Preeclamptic condition is often associated with throbbing headache [2]; when patients present a severe, unusual headache, the so-called thunderclap headache, a prompt investigation is necessary; a subarachnoid hemorrhage could justify the symptom [3].

In patients who underwent spinal anesthetic procedure, a new headache episode could be related to low intracranial pressure due to a CSF leak; the headache typically begins 1–7 days postpartum [4].

Pregnant patients with transient motor, sensory, or visual symptoms commonly have migraine with aura. The neurological symptoms are reversible and disappear in 20–30 min [1].

Pregnant or postpartum women with seizures can be grouped into three categories: an established seizure disorder before pregnancy, new nonpregnancy-related seizures disorder (brain tumor or hypoglycemia), and new seizures that are pregnancy related (eclampsia, PRES, cerebral venous thrombosis) [1].

15.2 Cerebrovascular Complications

15.2.1 Posterior Reversible Encephalopathy Syndrome (PRES)

Posterior reversible encephalopathy syndrome (PRES) is an acute rapidly evolving clinical condition described in 1996 by Hinchey et al. [5], characterized by headache, nausea and vomiting, abnormalities of visual perception, altered alertness and behavior, mental status abnormalities, seizures, and occasionally focal neurological signs [2].

The majority of case reports are found in the obstetric and gynecology literature and are associated with obstetric patients suffering from preeclampsia or eclampsia. A large proportion of these patients present in the immediate postpartum period, although they can present before delivery [2].

Initially described in the setting of preeclampsia/eclampsia of pregnancy and interruption of antihypertensive therapy, other causes were described in the development of PRES, as hypertensive encephalopathy, renal disease, and neurotoxicity of cyclosporine A or other immunosuppressive drugs [6].

Preeclampsia is one of the most common situations described in association with PRES. It is a multisystem disorder due to an abnormal placentation. Eclampsia, the major neurological complication of the preeclampsia, is defined as a convulsive episode or any other sign of altered consciousness arising in a setting of preeclampsia. Delivery is the only curative treatment for preeclampsia [7].

An important characteristic of PRES is the reversibility of the imaging abnormalities within days after appropriate therapy. If appropriate management is delayed, there is a high risk of permanent neurologic damage secondary to cerebral infarction or hemorrhages [8].

Essentially, the diagnosis of PRES is retrospective. Significant reversal of neuroradiologic abnormalities is suggestive of diagnosis. MRI played a decisive role in the diagnosis of PRES.

Specific MR abnormalities have been described in patients with PRES including extensive symmetric bilateral hyperintensity in T2-weighted images of parieto-occipital subcortical white matter and in the corresponding cortical regions [6] (Fig. 15.1a, b).


Fig. 15.1

PRES in woman of 28 years old on the 7th month of pregnancy. The patient complains of seizures and hypertension. In FLAIR images (a) bilateral and symmetric hyperintense areas in parietal-occipital regions were evident. In (b) the follow-up exam (after 10 days) is evident with normalization of cerebral tissue intensity

Involvement is usually symmetric, but the degree of involvement may be asymmetric [2] (Fig. 15.2a–h).


Fig. 15.2

PRES and low CSF pressure syndrome after delivery and spinal anesthesia. Woman of 30 years old. Three days after delivery, the patient complains of seizures and orthostatic headaches. In MR images, there is evident cerebral vasogenic edema in the parietal-occipital and, to a lesser extent, in the frontal lobes bilaterally (ac). Reduced ventricular volume and dural enhancement after gadolinium (d) are evident. After 15 days, a disappearance of brain lesions and a normalization of ventricular volume are noted (eh)

Signal alterations can also occur to a lesser extent in the basal ganglia, posterior temporal and frontal lobes, corona radiate, brain stem, and cerebellum [67] (Fig. 15.3a–e).


Fig. 15.3

Cerebellar location of PRES in woman of 30 years old on the 6th month of pregnancy. Vasogenic edema (ab) in both cerebellar hemispheres is associated with light enhancement after gadolinium (c). No evidence of reduced diffusivity is visible (de)

Evaluation with diffusion-weighted images of patients with PRES show increased diffusion with elevated values of ADC due to the presence of vasogenic edema. Nevertheless, there have been described cases of coexistence of vasogenic with cytotoxic edema [6].

Even though most reports have underlined a white matter predilection, Casey et al. in a recent study showed that cortical lesions are more common than what is previously thought [79].

Patients with seizures rarely had involvement of cortical matter; patients with autoimmune disease were more likely to have cerebellar involvement; patients with sepsis or active infections were more likely to have cortical involvement [10].

Comparing pregnant and nonpregnant patients, despite some clinical significant differences in pregnant women, headache and visual disturbance are more common than in nonpregnant patients [11]; no other significant differences are reported about the topographic distribution of cerebral lesion. In both group, common areas involved by the lesions are occipital and parietal lobes, followed by frontal and temporal regions [10].

Pathophysiology of PRES is still incompletely understood.

One proposed mechanism is that hypertension induced potentially reversible vasospasm, especially of posterior border zone territories, characterized by cytotoxic edema which can possibly evolve to ischemic lesions if not successfully treated [6]. Occasional angiographic evaluation of women with preeclampsia/eclampsia documented widespread intracranial vessel vasospasm [12]. On the other hand, several considerations are in contrast with this hypothesis. If we accept arteriolar vasospasm and distal ischemia as the principal alteration, the acute lowering of mean arterial pressure should further reduce perfusion to these regions; however, most patients respond well to antihypertensive therapy and ischemic infarctions are fairly rare [6].

An alternative theory, which has been best characterized in preeclampsia, eclampsia, and sepsis, implicates endothelial dysfunction [10].

The third and now widely accepted hypothesis considers the altered status of cerebral perfusion autoregulation.

Brain perfusion is maintained constant by an autoregulatory system consisting of a myogenic and a neurogenic response (sympathetic innervation). The transient disruption of the cerebral autoregulation with forced dilatation of arterioles causes leakage of serum through capillary walls into the cerebral interstitium [268].

The functionality of the autoregulation can be expressed as the autoregulatory index (ARI), with 0 being absent and 9 perfect cerebral autoregulation. This ARI has been shown to be lower in preeclampsia when compared with normotensive control subjects [14].

The principal posterior distribution of white matter alterations has been attributed to the sympathetic innervation of the cerebral vessel which accounts for the neurogenic response of cerebral autoregulation to hypertension.

This distribution has an anteroposterior gradient with a relative reduced innervation of the posterior cerebral arterial circulation. During acute elevation of blood pressure, posterior brain regions may be particularly susceptible to breakthrough of autoregulation.

It has been proposed that the fluid accumulation often observed during pregnancy, particularly in the third trimester, may accentuate the increase in development of vascular endothelial permeability in the brain. An increase in permeability can promote under hypertension [8].

Cortical blindness is a rare and dramatic complication of preeclampsia. Petechial hemorrhages and focal cerebral edema in the occipital cortex secondary to ischemic injury and vasogenic edema causing increased capillary permeability are considered to be important factors for the pathogenesis of cortical blindness in preeclampsia [15].

PRES has been less commonly described in the setting of autoimmune disease. The distinctive role of autoimmune disease is often clouded by concurrent hypertension, renal disease, and the use of immunosuppressants [10]. In autoimmune disorders, PRES is in part caused by endothelial dysfunction due to an inflammatory cytokine response that leads to autoimmune-mediated disruption of the endothelial aquaporin 4 water channels [10].

It is known that a woman who develops preeclampsia has a higher risk of developing cardiovascular disease later in life, as hypertension, ischemic, and hemorrhagic stroke. This condition leads formerly preeclamptic women to have cerebral white matter lesions more often and more severely than control women with normotensive pregnancies. Preeclampsia appears to be an independent risk factors for white matter lesions, and this was predominant in women with early-onset preeclampsia [16].

Another study assessed that an episode of PRES may play an additional role in increased prevalence of cerebral white matter lesions, visible in frontal lobes rather than in occipital lobes. Severe vasogenic edema has been suggested to potentially progress to such an extent that regional perfusion decreases, leading to areas of cytotoxic edema, infarction, and development of white matter lesions in the long term. In the same study, the authors reported that white matter lesions are more common in women with prior pregnancies complicated by preeclampsia or eclampsia compared with parous women in a control group [16].

Other two pathologic conditions are reported in pregnancy-related vascular encephalopathy: HELLP (hemolysis-elevated liver enzymes-low platelets) syndrome and RCVS (reversible cerebral vasoconstriction syndrome) [18]. The first is associated with strong epigastralgia, hepatic failure, disseminated intravascular coagulation, and intracerebral hemorrhage. The syndrome is caused by low placental gene expression of nitric oxide. Generally, MR imaging findings of HELLP syndrome may overlap with those of PRES (cerebral edema), with prevalent involvement of basal ganglia and brain stem [19]. Lacunar lesions are frequent [18].

Typical symptom of RCVS is a “thunderclap” headache due to multifocal or segmental cerebrovascular spasm, visible on MR angiography, which resolved within 12 weeks. Parenchymal lesions are frequently located in areas of the anterior circulation [18].

15.2.2 Ischemic Stroke, Venous Thrombosis, and Cerebral Hemorrhages

There is an increased risk of strokes in pregnancy and puerperium. Intracranial hemorrhage is secondary to hypertensive disorders of pregnancy with smaller proportions related to aneurysm and arteriovenous malformation rupture. A small but important contributor is cortical venous thrombosis. Presentation is usually with headaches or seizures, with or without focal deficits [20].

Pregnancy and the puerperium are considered hypercoagulable states. The risk of both ischemic infarction and intracranial hemorrhage increased with age and is high in the peripartum period and puerperium, but not during the pregnancy [21].

Cerebral venous thrombosis may occur anytime during the course of pregnancy and the puerperium, but the risk is high during the first 2 weeks of the puerperium. Venous sinus hyperdensity on CT acquisition and loss of venous flow-void artifact on MR images are typical findings (Fig. 15.4a–e). Venous infarcts do not represent the arterial territories and are often associated with hemorrhage at the gray-white matter interface [22].


Fig. 15.4

Venous thrombosis in a young woman on the 3rd month of pregnancy. Hyperdensity of transverse and sigmoid sinus are evident (aarrow); loss of enhancement into the sinus after contrast injection (delta sign, barrow). MR investigation confirms venous thrombosis in contrastographic MR angiography study (c) and in FLAIR (d), T2- (e) and T1-weighted (f) images where the venous structures show high signal

Subarachnoid hemorrhage (SAH) is the third most important cause of maternal mortality during pregnancy in the United States. Maternal mortality due to rupture of an intracranial aneurysm ranges from 13 to 35 % [23].

The frequency of aneurysmal SAH during pregnancy increased with advancing gestational age, with more than 50 % of intracranial aneurysm ruptures occurring in the third trimester [24].

This condition is related to the gravid state: increases in blood volume and blood pressure and hormone’s increase. It is reported intracranial aneurysm formation, enlargement, and rupture during pregnancy [25]. The common site of intracranial aneurysm is the internal carotid artery [24].

MR angiography represents a screening technique able to discover intracranial vascular lesions [23].

Vascular malformations such as arteriovenous malformations, moyamoya disease, and cavernous malformations undergo morphological changes under the influence of female hormones and increase of blood levels of vascular growth factors that lead to an increase of incidence of bleeding [26].

15.3 Tumors

The frequencies of brain tumors appear to be similar for pregnant and nonpregnant women [27], whereas pregnancy seems to be involved in growth of some intracranial tumors.

Many studies report that pregnancy is associated with meningioma growth, due to the common expression of progesterone and estrogen receptor [28]. This was first recognized in the 1930s and documented in multiple reports of women with meningiomas who had symptom onset during pregnancy and remission during the postpartum period [29]. Other intracranial tumors that show dimensional increases during pregnancy are hemangioblastoma and vestibular schwannoma.

Large cohort studies show pregnancy by itself does not influence the risk of developing a glioma [30].

However, the role of pregnancy about the growth of gliomas is debated. Some authors reported that pregnancy has no significant effect on the incidence or behavior of glioma [21]; others assessed that the pregnancy may influence glioma behavior and the glioma may affect the course of pregnancy [30].

Other authors referred that in pregnant women with no clinical signs of glioma progression, detailed neuroimaging may well show an increase in tumor volume [30].

These phenomena are probably correlated with increase of blood volume due to hormonal increase that leads to exacerbated peritumoral edema and increase in mass effect. This mechanism could explain a return of tumor mass to prepregnancy volumes following delivery [30].

Two small retrospective case series described a potential impact of pregnancy on gliomal growth and transformation to higher-grade tumors [3132]. Similar results are reported about meningiomas [33]. The increased growth rate was associated with a higher frequency of seizures, and it is linked to the hormones and growth factors increase.

Several theories have been proposed to explain the progression of brain tumors during pregnancy. Hormonal changes and increases in the levels of growth factors and angiogenic factors during pregnancy influence the rate of growth of brain tumors [34]. Increased levels of vascular endothelial growth factor (VEGF) and placental growth factor are well-established angiogenic factors in GBM [35].

In a recent study, the authors reported that grade I gliomas remained stable during and after pregnancy. The different tumor biologies, characterized by minimal tumor infiltration and absence of angiogenesis, could explain the absence of tumor progression [36].

The link between brain tumors and hormones is known.

Tumor growth for specific tumors was found to depend on the stage of the pregnancy with meningiomas in the third trimester and gliomas in the first trimester [29]. The appearance of de novo high-grade gliomas in healthy pregnant women occurred mostly in the late second and third trimester [30].

Meningiomas more frequently express progesterone and glucocorticoid receptors; higher levels of progesterone receptors have been observed to be higher in GBMs as compared to anaplastic and low-grade astrocytomas [29].

15.4 Pituitary Disorders

Pituitary apoplexy is extremely rare during pregnancy and has been reported in only a few cases in the literature [37].

During pregnancy the normal pituitary gland undergoes physiological adaptations to meet the increased metabolic demands of the maternal-fetal unit [21].

Magnetic resonance imaging (MRI) showed that the pituitary volume may increase by 45 %; mean height of normal gland during pregnancy is 9.6–10 mm and in immediate postpartum 10.2–12 mm (Fig. 15.5a–d).


Fig. 15.5

Pituitary apoplexy. Woman of 27 years on the 2nd month of pregnancy. The patient aborts and complains severe headache and hyperprolactinemia. The MR study shows a volumetric increase of the pituitary gland with hemorrhagic area on the right (abd). Bleeding of a pituitary microadenoma was suspected in (c) the normal pituitary enhancement after gadolinium doesn’t allow to distinguish the hemorrhagic area

During pregnancy the maternal pituitary gland undergoes remarkable hemodynamic changes. Increase in size of the pituitary gland is associated with increase in number of lactotroph cells and a physiological increase in serum prolactin production. The placental estrogen enhances the same process. If a pituitary adenoma coexists, blood supply to the tumor may cause infarction or hemorrhage.

MRI is an essential diagnostic tool, confirming the diagnosis of pituitary apoplexy in over 90 % of the patients [38].

Pituitary apoplexy is related to hemorrhagic infarction of pituitary gland with variable association with intracranial hypertension, ophthalmoplegia, and panhypopituitarism [3940]. Often it is associated to a preexisting adenoma, although in few cases apoplexy is reported without pituitary pathology, such as Sheehan syndrome [41].

The most common symptom is headache with an incidence of 90–97 %; this is often described as a sudden, severe head pain, frequently with retro-orbital location [3940]. This “thunderclap headache” is similar to subarachnoid hemorrhage, cerebral venous thrombosis, or cervical artery dissection [3]. Other common symptoms are visual deficit, nausea, vomiting, ocular palsy, and meningism.

Although most of patients undergo computed tomography in emergency phase, this technique demonstrated a low sensitivity in detecting pituitary hemorrhage [42]. A possible explanation is related to similar hyperdense pathologies that involve the gland, as aneurysm, Rathke cleft cyst, germinomas, or lymphomas. Another reason is the blood degradation that confounds diagnosis in the days following the acute onset of symptoms.

MRI predominantly showed an intra- and suprasellar expanding mass with different signal intensities on T1WI and T2WI, depending on the presence of hemorrhage and on its stage.

Hyperintensity on T1-weighted images, inhomogeneous signal on T2-weighted images, and slight contrast enhancement after gadolinium are typical findings inside the gland [43].

A thin peripheral ring of marked hypointensity representing hemosiderin could be visible on T2- and T2*-weighted gradient echo; this is an unexpected finding, since pituitary tumors lack a blood-brain barrier, and the accumulation of macrophages containing hemosiderin normally does not occur [44].

The presence of fluid debris level within the mass, suggestive of late subacute hemorrhage, and the thickening of sphenoid sinus mucosa, related to venous engorgement, are important MR findings indicative of pituitary apoplexy [45].

A rare condition of pituitary apoplexy without hemorrhagic infarction has been described: low signal intensity on both T1WI and T2WI without contrast enhancement inside the lesion but with a peripheral rim of enhancement could be evident [46].

Many other pathologic conditions can imitate a pituitary apoplexy. Aneurysm arising from the carotid siphon, Rathke cleft cysts, craniopharyngioma, lipoma, or dermoid cysts could show hyperintensity on T1-weighted images similar to pituitary apoplexy. Often clinical history and symptoms could help in differential diagnosis performing.

Sheehan syndrome is a clinical state of panhypopituitarism due to pituitary infarction that occurs after an obstetrically related hypotensive episode around the time of delivery. At imaging, there is usually the appearance of a partial or complete empty sella [2141].

Lymphocytic adenohypophysitis is a rare inflammatory disorder of the anterior lobe of the pituitary gland that may affect young women in the peripartum. Postpartum hypoprolactinemia is attributed to pituitary parenchymal damage caused by the severe inflammatory reaction. At imaging, there is enlargement of the gland with suprasellar extension; an early enhancement after gadolinium and thickening of the infundibulum complete the adenohypophysitis pattern [21].

15.5 Multiple Sclerosis

The influence of pregnancy in multiple sclerosis is debated. Women with multiple sclerosis were discouraged from contemplating pregnancy due to the possible dangerous effect of pregnancy on multiple sclerosis [47].

The relapse rate decreased significantly during pregnancy, especially in the third trimester, and increased in the first trimester after delivery [4748]. The disease activity of multiple sclerosis is known to decrease during pregnancy. Estrogen levels increase during pregnancy, and basic research have shown that estrogens have immunomodulatory effects on immune cells [49].

From the second trimester and for the following 21 months, the annualized relapse rate fell slightly but did not differ significantly from the relapse rate recorded in the prepregnancy year [47].

An increased relapse rate in the prepregnancy year, an increased relapse rate during pregnancy, and a higher disability status scale score at pregnancy onset significantly correlated with the occurrence of a postpartum relapse [47].

The possibility of future pregnancies in female patients with multiple sclerosis has to be considered in their clinical and therapeutic management: the advantages of a drug have to be balanced with the possible effects on fertility, gestation, and fetal outcome. Time and modality of suspension of the drug in case of pregnancy planning should be also considered [50].

Some cases of resumption of disease activity after delivery are reported because of the interruption of drug administration (i.e., natalizumab) [50].



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