2 19
Correlation of CT Cerebral Vascular Territories with Function: II. Posterior Cerebral Artery
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L. Anne Hayman 1,2 This paper presents schematic displays of the cerebral territories supplied by Stephen A, Berman3 branches of the posterior cerebral artery as they would appear on axial and coronal Vincent C, Hinck2 computed tomographic (CT) scan sections. Companion diagrams of regional cortical function and a discussion of the fiber tracts are provided to simplify correlation of clinical deficits with coronal and axial CT abnormalities. Illustrations of the vascular supply and functional relay points (nuclei) of the thalamus are provided,
Thi s report is th e second in a seri es designed to correlate cerebral vascular territories and functional anatomy in a form directly applicabl e to computed tomography (CT) [1]. The illustrations are intended to simplify analysis of CT images in terms of clinical signs and symptoms and vascul ar territori es in everyday practice. Knowledge of vascular territories can help in differentiati on between infarcti on and other pathologic processes. For example, if th e position and extent of a lesion and the usual position and extent of a vascular territory are incongru ous, infarction should receive relatively low diagnosti c priority and vi ce versa. Knowl edge of vascular territories can also facilitate correct interpretati on of cerebral angiograms by pinpointing specific vessels for parti cularl y c lose attention. Knowledge of functional neuroanatomy applied to a pati ent's clinical features can improve detection of subtle lesions by pinpointing specific territori es for Received December 8, 1980; accepted Janu ary 9, 1981 special attention on CT and spec ific vessel s for attention on angiograms. This work was supported in part by EMt Med. tnc. ' Department of Radiotogy, U.S.A.V. Hospita t, Discussion Houston, TX 772 11 , and Suite 2026, University of The vascular territori es of th e posteri or cerebral artery and the neurologic functions Texas Medicat School, 6431 Fannin 'St., Houston, TX 77030. Address repri nt requests to L. A. Hay ascribed to those territori es are mapped on schemati c axial and coronal ' CT scans (figs. ma n. 1 and 2), and on maps of th e medial surface of th e cerebral hemisphere (fi g. 3). Th e 2Department of Radiotogy, Bay tor Cott ege of branches of th e posteri or cerebral artery have been divided into three groups: (1) the Medicin e, Houston, TX 77030. penetrating arteri es to the brain stem, thalamus, and other deep structures. (2) th e spleni al 3Department of Neurotogy, Baylor Co tt ege of branch to the corpus call osum , and (3) the branches to the cerebral hemisphere [3]. Medicin e, Houston, T X 77030. This artic te appears in May/ June 198 1 AJNR and July 198 1 AJR . Penetrating Branches
• The plane of coronal CT scans obtained de Numerous very small branches ari se from th e proximal part of th e posterior pends on head positioning. If th e coronal im age is a reconstruction, th e pl ane is perpendicular to th e cerebral artery as it encirc les th e midbrain . These have arbitrarily been divided axial scans whi ch may va ry in their slope. There into one group that supplies th e thalamus and hypothalamus and another that fore, we have chosen to ittu strate th e vascular territori es in the anatomic coronal plane. The supplies the midbrain [3]. reader must correct for minor diHerences in scan Thalamus and hypoth alamus, The approximate origin and term ination of th e ning angle. This witt be facilitated by a review of vessels that supply the th alamus are indicated in fi gure 4 A. Each vessel in th e coronal slic es ittustrated by Matsui and Hirano [2] drawing represents numerous very small branches. The pattern of arterial suppl y AJNR 2 :219-225, May/ June 1981 to the th alamus is vari abl e; th at shown in figure 4A is th e most common, 0 195- 6 108 / 8 1/ 0203-02 19 $00.00 © American Roentgen Ray Society representing 30% of the brains studied by Schl esinger [3]. In general, four Fig . 1 .-Axial CT scan diag rams arranged in sequence from base to verlex. Angle and levels of scan planes are shown in fig . 3. Territory of posterior cerebral artery is divided inlo Ihree regions: Ihalamic and midbrain perforalors (m edium blue) callosal (dark blue) and hemispheri c (Iighl blue).
Fig. 2. -Coronal CT scan diagrams arranged in sequence from fronl to back. Angle and levels of scan planes are shown in figure 3. Terrilori es of posteri or cerebral artery are identified as in fig . 1 . AJNR:2, May / June 1981 CT OF POSTERIOR CEREBRAL ARTERY 22 1
A o H K N a T V CO l pus call osum -- -
i1. P'l'milmillary -- b. Thalamoperlorators c. Thalmogen.culale
d, PostE- ri O' chol oldal --12 and clngu late hlanch
V I EW FROM ABOVE A
--1
---12 A
Corpu~ call osum B - --4 '~a l elllle~~-"'- " -~~"~" 2 , -...... 2 Mo.o, ... b,I"",oo -~--.. L;'G T G 3 Senl
VI SUAL FIELD DEFICIT V I EW FROM BELOW ~ ____ OPtIC Iract ()() ~ ____ Geniculille body Rt . homonymous hemianopsia
Optic rad.atlom of the lower ~ cal ca rine cortex (CUi surface) RI. homonymous superior quadrant
OptiC radiatiOns 0 1 the upper calca rine cortel( RI. homonymous Inferio r quadrant
5 6 Fig. 5 .-Postinfusion axial CT scan (at scan level 4 of fig . 1). Infarction of Fig. 7.-Visual pathways viewed from be/ow. Visual defects produced by anterior aspect of right thalamus, which is usually supplied by premamillary lesions along left optic tract. Radiations are very close to ventricular walls. branches of posterior communicating artery (area a in fig 4A). Patient had sudden onset of severely diminished mental ability and motivation (area 1 in fig . 48). Psychiatric eva lu ation suggested organic cause for disability, promptin g CT evaluati on. rior lateral and ventral posterior medial nuclei relay sensory Fig. 6.-Axial CT scan (at level 5-6 in fig . 1). Enhancing infarction (arrow) information from body and face, respectively [4]. Lesions in th alamogeni culate territory (area c in fig . 4A). Patient had Dejerine-Roussy (thalamic) syndrome of altered sensation (area 3 in fig. 48). produce an initial insensitivity to pain that evolves over a period of months into spontaneous or inappropriately elic ited pain in the affected body part. This has been named hormone releasing factor, corticotrophic releasin g factor, anesthesia dolorosa and is found in the Oejerine-Roussy and prolactin inhibitory factor [1 2] travel through this region. (thalamic) syndrome [16] (see figs. 4 and 6). Therefore, intermediate hypothalamic lesions can cause a The thalamogeniculate branches also supply the lateral complete loss of endocrine function, simulating total section geniculate body, the medial geniculate body, and structures of the pituitary stalk. Lesions in this area cause hyperphasia, below the anterior and medial part of the thalamus (e.g., anorexia, and rage attacks [11]. Forel fields in the subthalamic area). Lesions of the lateral The premamill ary artery together with branches from the geniculate body cause loss of sight in the half of the visual thalamoperforating arteries also supplies the posterior part field opposite the lesion [4] (see figs. 7 and 8). The medial of the hypothalamus [10]. Tumors in this area produce geniculate body is part of the hearing pathway but unilateral precocious puberty [11], disturbances of temperature reg lesions of the medial geniculate body do not cause clinical ulation [13], and disturbances of consciousness with som hearing problems since there is bilateral representation of nolence [11]. (The anterior hypothalamus forms the an terior hearing at this level due to previous decussation. Lesions in walls of the third ventricular chamber and influences tem the vicinity of the subthalam ic area and Forel fields can perature regulation, fluid electrolyte balance, synchroniza cause violent flinging movements of the opposite extremities tion of sleep and wakefulness, and perhaps some aspects call ed hemiballismus as well as the uncontrollable jerking of cardiac rhythm. It is supplied by small perforating and writhing movements of choreoathetosis [17, 18]. How branches from the anterior cerebral artery; infarctions in this ever, onl y hemiballismus has good localizing value and area can cause abnorm ality in any of its functions.) suggests a lesion in the nucleus subthalamicus. Since the As illustrated in figure 4A, the thalamoperforating arterial subthalam ic region receives coll ateral supply from the an group (b) supplies the medial ventral part of the thalamus terior choroidal artery, these manifestations are rare in (centromedianum and parafascicular nuclei). This territory infarction but common in hemorrhage [18]. mediates many aspects of arousal, attention, and alertness As shown in Figure 4A, the choroidal and cingulate [4]. Thalamoperforating branches derived from one poste branches (d) supply the posterior and superior thalamus rior cerebral artery commonly supply all or part of th e (anterior, medial, pulvinar, and habenular nuc lei). There are contralateral territory as well as the ipsilateral territory extensive anastomoses in these areas [14, 19] and infarc [14 ]. tion is rare. Symptoms resulting from lesions in the first As illustrated in Figure 4A, th e thalamogeniculate group three of these thalamic nuclei have been described in the (c) supplies the lateral ventral part of the thalamus (pulvinar, previous discussion. There is no known specific c linical ventroposterior lateral, and ventroposterior medial nuclei). deficit produced by habenular lesions per se. In addition to The pulvinar may coordinate visual and auditory information th e thalamus, the posterior choroidal branches supply the by receiving input from the lateral and medial geniculate pineal, c horoid plexus, crus, commissure, and body of the bodies and projecting to the occipital and temporal lobes fornix, part of the anterior columns of the fornix, and part of [4]. Lesions of the left pulvinar area can produce language the lateral geniculate body [14]. dysfunction (aphasia or dysphasia) [15]. The ventral poste- Midbrain . The second group of small penetrating AJNR:2, May/ June 198 1 CT OF POSTERIOR CEREBRAL ARTERY 223
Fig. 8.-Axial contrast CT scans (levels 3 -7, fig. 1). Enhancing infarction of cortex supplied by left posterior lem poral, calcarine, and parietooccipital ar leries, and th alamogeni culate territory (arrow), which includes medial part of lateral geniculate (arrowhead). This pro duced loss of entire right half visual field (contralateral homonymous hemianopsia (see fig. 7). Sensory changes were nom inal. Also, note infarction in distribution of prefrontal branch of right middle cere bral artery.
A B c branches supplies the midbrain [19]. They enter the mid gether. Isolated brain stem lesions involving a single third brain substance perpendicularly, either directly at their point nerve nucleus are therefore very rare (see fig. 4B). Brain of origin from the posterior cerebral artery or after accom stem lesions may simulate peripheral third nerve lesions by panying the parent artery around the midbrain for some compromising nerve fibers in the brain stem before they distance [19, 20]. Others term these " thalamoperforators" exit. Some authors have stated that third nerve paralysis and the syndromes produced by their occlusion " thalamo without pupillary abnormality indicates infarction rather than perforate syndromes" [21]. Since this group of vessels does compression by a mass, but this distinction is unreliable not supply the thalamus it would be better to call them [23-26]. " midbrain perforators" and the associated syndromes There are fibers of the third nerve at the collicular level of " midbrain perforate syndromes." the midbrain that can be damaged by tumor compression The midbrain contains many vital pathways and nuclei; (e.g., pinealoma) producing Parinaud syndrome, lesions here have a variety of clinical manifestations. Some [26, 27]. This consists of loss of upward gaze, impaired of these deficits have eponyms (e.g., Claude, Nothnagel, pupillary reactivity, and convergence nystagmus, which is Weber, and Benedikt syndromes, among others). There is not true nystagmus, but, rather, a simultaneous contraction disagreement in the literature as to the precise constellation of all the extraocular muscles. Convergence results because of symptoms found in each of these syndromes, so these the medial recti are the strongest muscles of the group eponyms will not be used in our discussion [19, 21, 22]. [26]. Only a combination of deficits can be used to localize a Disturbances of sensation or movement are caused by lesion to the brainstem, because an isolated lesion in struc damage to the major sensory tract (medial lemniscus) or tures outside the midbrain can produce identical deficits. It motor tract (pyramidal) (see figure 4B). Lesions here cause is the combination of deficits that enables localization of a contralateral hemianesthesia and / or hemiparesis and may lesion to the midbrain. Lesions within or pressing on the affect the head (H), arm (A), or leg (l) in varying degrees midbrain produce identical symptoms by compromising one [28]. or more of the vital centers in the midbrain. Therefore, the Damage to the red nucleus, which coordinates cerebellar etiology cannot be determined by clinical means. thalamic fiber tracts (see fig. 4B), results in impaired coor Damage to parts of the midbrain can lead to: (1) third dination and control of movement contralaterally [29]. There nerve paralysis causing symptoms in both eyes but most is tremor during movement (perpendicular to the direction marked in the eye on the same side as the lesion; (2) of motion) that worsens as the target is approached. One disturbed sensation, strength, and/or coordination on the also finds dysmetria, difficulty with rapid alternating move side opposite the lesion; (3) depression of consciousness; ments and inability to check or stop a previously initiated and (4) decerebrate rigidity. A detailed description of these movement [27, 30, 31 ]. Another related type of tremor, deficits follows. The reader will find it helpful to refer to rubral tremor, may also be seen. This tremor is present at figure 4B to visualize the position of the third nerve nucleus, rest, although it increases during movement. It involves the red nucleus, and motor and sensory tracts in the midbrain limb more proximally than does the usual cerebellar tremor. as these structures are discussed. A third type of tremor, seen only at rest, which is similar to A total third nerve paralysis results in ptosis, a dilated that seen in Parkinson disease, may also be encountered unreactive pupil and downward and outward deviation of [27, 30, 31]' In addition to the tremor, there may be contra the eye ipsilaterally. Injury to peripheral third nerve fibers lateral hemiballismus and choreoathetosis (as described (after they leave the brain stem or as they travel through the previously) if there is damage to the adjacent substantia cisterns to reach the eye) causes some or all of these nigra and / or subthalamic region [21, 29, 30, 32]. symptoms ipsilaterally. Brain stem lesions may cause third Depression of consciousness is presumably caused by nerve symptoms bilaterally since the nuclei are close to- damage to the central or paramedian reticular midbrain 224 HA YMAN ET AL. AJNR:2, May/ June 1981
Fig. 9 .-Axial CT scan (level 2 , esting c linical syndromes. The calcarine artery (sometimes fig . 1). Left midbrain infarction (ar together with the parietooccipital artery) supplies the cal row). Patienl had right hemiparesis with facial sparing and dysarthria carine cortex on one side. Infarction thereof causes homo and left third nerve palsy, later re nymous hemianopsia of the contralateral visual fields (fig. solved, bul right-sided sensation 8). It is commonly stated that, with lesions of the calcarine remained impaired. There is only a partial correlation between ac cortex, the central macular part of the visual field is spared tual deficits and those based on due to collateral circulation [35). We have rarely seen this. fig . 48. Infarction of the calcarine cortex bilaterally results in complete blindness. However, there is sometimes also an unusual constellation of symptoms known as Anton syn drome in which the patient, although blind, is unaware of the blindness and denies it [36). Sometimes he will construct elaborate descriptions of his surroundings. If allowed he will often walk into walls or trip over objects. Patients sometimes also display difficulty in tactile identification and enumera tion of objects. Apraxia of occular movements may also be encountered. It is in bilateral occipital infarction th at macular sparing is most commonly reported. Macular sparing in activating system. It can be also caused by destruction or these instances may actually represent partial recovery from depression of the retic ular system in the pons or medulla or total blindness [34). Damage to the calcarine cortex can by bilateral hemispheri c dysfunction. This impairment of also produce unformed visual hallucination, metamorphosia consciousness is of little localizing value [27). (distortion of shape), teleopsia (an illusion in which near Decerebrate rigidity can be produced in animals by le objects appear to be at a great distance), distortion of visual sions in the regulating structures between the quadrigeminal outlines, and other aberrations of visual perception [36). plate and the lateral vestibular nucleus in the pons [27, Damage to the nondominant calcarine cortex as well as 33). The subject assumes a position in which the legs are damage to the nondominant lingual gyrus, which are sup rigidly extended and th e arm s are extended, adducted, and plied by the calcarine and temporal branches (fig . 38), may hyperpronated [25). This posture is not as reliable a local produce topographic disorientation and prosopagnosia. izing indicator in humans as it is in other animals [23). Prosopagnosia is the inability to recognize familiar faces In our experi ence, CT of midbrain infarctions has not even though they can be clearly seen [36). correlated well with the clinical presentations. This may be Damage to the cortex above and below the calcarine due to brain stem damage not demonstrated by CT (see fissure, particularly in the dominant hemisphere, destroys figs. 48 and 9). the visual association areas that control involuntary eye function and visual comprehension (see fig . 38). These Ca llosal Branches areas are supplied by the parietooccipital and posterior temporal branches of the posterior cerebral artery. Patients The call osal arteries are a plexus of small vessels that with lesions in these areas rarely may continue for several arise from the parietooccipital or lateral choroidal branches seconds to see th e image of an object that is quickly and penetrate the upper surface of the posterior one-half of removed from view. They may also not perceive an object the corpus call osum. The plexus may be replaced by a in the damaged visual field if another identical object is si ngle branch [14). Infarction can result in separation of the simultaneously presented in the normal visual field . This language-dominant left hem isphere from the ri ght hemi phenomenon is called extinction [36). sphere, which mediates function of the left side of th e body. The anterior temporal branch supplies only the inferior If the patient's left occipital lobe and splenium are infarcted, aspect of the anterior temporal lobe; the tip of the temporal he can speak, write, and understand speech but he be lobe is supplied by the middle cerebral. The cortex in this comes unable to read with his remaining left visual field area is involved in naming objects. despite the fact that he can see the letters. (He cannot The hippocampal branches of th e posterior cerebral ar transfer the visual images received by th e right occipital tery supply the hippocampal formation including its projec lobe for interpretation in the left hemisphere.) This is call ed tions, the fornices, and th e psalterium (fig. 3 8). The most al exia without agraphi a. It is rare and may be partial [34). commonly observed clinical finding in patients with bilateral hippocampal infarcts is memory deficit. This may also be seen with unilateral deficits on the dominant side. Lesions Hemispheric Branches in this area may also impair the sense of smell [36). The posterior cerebral artery has five corti cal branches. The functional neuroanatomy and vascular territories sup The patterns of infarction can be simplified by comparing plied by the posterior cerebral artery have been graphically the vascular territories (fig. 3A) with the corresponding summarized in a format directly appli cable to CT to simplify functional areas (fig . 38). Infarction of cortical branches of correlation of CT images, c linical signs and symptoms, and the posterior cerebral artery is responsible for several inter- vascular territories in everyday practice. We hope this infor- AJNR :2, May/ June 1981 CT OF POSTERIOR CEREBRAL ARTERY 225
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