Folia Psychiatrica et Neurologica Japonica, Vol. 29, No. 4, 1975
Thrombosis of Rolandic Veins Following Lumbar Anesthesia: A Case Report Kazuki Sakata, M.D., Hiromu Yamada, M.D., Takeshi Chujo, M.D., Tatsuhiko Abe, M.D. and Juji Tsuchiya, M.D. Second Department of Surgery, G i f u University School of Medicine, G i f u
INTRODUCTION The syndrome of occlusion of the rolandic veins, unaccompanied by occlusion of the superior sagittal sinus, has been described by Menvarth5 and various later authors. However, occurrence of the syndrome following lumbar anesthesia seems to be quite rare. One such case, experienced by us, is reported. CASE REPORT
A 23-year-old female was admitted to our clinic on December 4, 1974, with chief complaints of convulsive attacks involving the right half of the body and paralysis of the right extremities. On November 21, or 13 days prior to admission, she noted right lower abdominal pain. Since the symptom did not improve, she consulted a surgeon and, being diagnosed as acute appendicitis, she underwent appendectomy under lumbar anesthesia on November 28. According to the surgeon her appendicitis was mild. Shortly after the operation she came to complain of severe headache, nuchal pain and nausea, which continued up to the time of admission to our clinic. On December 2, she noted motor disturbance of the right extremities and numbness sensation of the right half of Received for publication August 11, 1975,
the body. The motor disturbance was aggravated gradually, coming to show complete paralysis of the right extremities on December 3. In the next morning (the day of admission) an attack of clonic convulsion of the right leg, lasting for a few minutes, appeared, followed then by several attacks of tonic and clonic convulsions, involving the right half of the body and lasting for a few minutes at each time, on the same day. Consciousness was not impaired during the seizures. Her appetite was disturbed. Menstruation was regular and no oral contraceptive was used. She had no prior history of convulsion and her family’s medical history was nothing particular. On admission, her consciousness was clear. Systolic and diastolic blood pressures were 110 and 58 mmHg respectively. Severe left headache, especially in the occipital region, and neck stiffness were noted. Size of the pupils, light reflex, visual acuity and fundoscopic finding were all normal. Flaccid paralysis of the right extremities and slight weakness of the right facial muscles were noted. There was right sensory hemiparesis accompanied by paresthesia. Babinski reflex was positive on the right side. No abnormality was found in the abdomen except for a sutured appendectomy wound. Lumbar puncture, done on December 4, revealed that the cerebrospinal fluid (CSF) pressure was O m m of water, and the CSF,
356
K. Sakata
rt a/.
Thrombosis of Rolandic Veins
Fig. I (a and b): A-P view (a) and lateral view (b) of phlebogram. Arrows indicate sites of venous obstruction.
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easily obtained by suction, was watery clear place in the following order: distal portions and showed no pleocytosis. Culture of CSF of the upper extremity, proximal portions was negative. thereof, distal portions of the lower extremity At the time of admission, bleeding time and proximal portions thereof. and coagulation time were normal, white cell On December 14 (10 days after admiscount was 4,800per cu.mm., red cell count sion), all the symptoms, including headache, was 330x lo4 per cu.mm., hematocrit was nuchal rigidity, sensory and motor disturb28% and platelet count was 3 4 ~ 1 0per~ ances of the right extremities and right posicu.mm. Serum protein was 8.2 mg/dl, and tive Babinski reflex, completely disappeared serum electrolyte and blood glucose levels and she was neurologically normal. She was were normal. discharged on December 17 and is continuEEG, recorded on December 5 , showed ing to be well subjectively and objectively diffuse moderate slowing and amplitude of five months after her discharge. Right carodiffuse 6 to 7 per second regular rhythms tid angiogram, done after her discharge, was was somewhat lower on the left side. No found to be normal. seizure discharge was noted. Left carotid angiogram, done on DecemDISCUSSION ber 6, revealed on phlebogram that the left rolandic veins were occluded near the porThe case presented here is a case of tion of their confluence to the superior sagit- thrombotic occlusion of the left rolandic tal sinus and collateral venous channels de- veins, which occurred four days after appenveloped (Fig. 1 a and b). In A-P view, the dectomy, done under lumbar anesthesia. Apleft side wall of the superior sagittal sinus pendicitis appeared to be mild and the opershowed some irregularities, suggesting pre- ation seemed to be uneventful, of course, sence of mural thrombi, but patency of the being unaccompanied by shock. Since no sinus was maintained sufficiently. Left serial marked fever was noted and there was no carotid angiogram, done on December 11, leucocytosis at the time of admission to our showed the same findings. clinic, a probability of infective cerebral Blood sedimentation rate, done on Decem- venous thrombosis, related to appendicitis, ber 7, was 16 mm in one hour and 43 mm in seems to be quite small. In view of the facts two hours. CSF pressure was found to be that headache, nuchal pain and nausea were recovered up to 65 mm of water on the same noted shortly after the operation and that the CSF pressure, measured on the day of day. After admission, she was treated by ad- admission, was 0 mm of water, it is certain ministration of anticonvulsant and hydro- that marked CSF hypotension following cortisone as well as intravenous infusion of lumbar puncture was present. It may be low molecular dextran solution. Convulsive reasonable to suppose that this CSF hypoattacks ceased on December 6. Toward that tension was etiologically related to thromtime, the formerly flaccid paralysis of the bosis of the rolandic veins. Dripps et a1.l describe headache, difficulright extremities became spastic, and voluntary movements of the extremities began to ties in hearing, ocular problems, traumatic recover. During the following several days, puncture and infection, as sequelae of lummotor palsy rapidly recovered and, simulta- bar puncture. They mention, further, that neously, right sensory hemiparesis disap- hypotension induced by lumbar anesthesia peared. The recovery of motor function took or hypoxemia due to respiratory failure may
Thrombosis of Rolandic Veins cause a reversible or irreversible impairment of the central nervous system, and that a central nervous system disorder may casually complicate, or a pre-existing such disorder may be aggravated by, lumbar anesthesia. They do not point out any possibility of occurrence of cerebral venous thrombosis, however. As far as we surveyed the literature, only one such case was found to be reported: i.e., Gabrielsen et al.“ reported a case of 40-yearold male case (their Case 4) who suffered from thrombosis of the superior sagittal sinus following appendectomy performed under lumbar anesthesia. No previous report has been found that occurrence of thrombosis circuinscribed to the rolandic veins following lumbar anesthesia, like in the present case, was observed. Relationship between CSF hypotension and cerebral venous thrombosis will next be discussed. It is generally known that the following factors contribute to formation of thrombosis: changes in blood properties, changes in vessel walls and slowing of blood flow. It is known that cerebral veins dilate as CSF pressure is reduced.’ Furthermore, it is considered that changes in relative position of the bridging veins interconnecting the cerebral surface and the superior sagittal sinus and consequent traction thereof, are important in causation of headache accompanying CSF hypoten~ion.~ Thus it is reasonable to suppose that the assumed retardation of blood flow within the dilated cerebral veins and/or retardation of blood flow within the portions of veins preceding the kinked or narrowed bridging veins, will facilitate thrombus formation. However, in view of rarity of cerebral venous thrombosis as a complication to CSF hypotension following lumbar puncture, its occurrence in the present case may be relevant to additive effects of other concomitant factors, such as anemia and dehydration
359
due to anorexia consequent on appendicitis and subsequent CSF hypotension. Anyhow, it is to be pointed out that, in case some symptom of central nervous system lesions occur following lumbar anesthesia, there certainly is a small probability, besides probabilities of sequelae of hypotension or hypoxemia during anesthesia, that the symptoms may be due to cerebral venous thrombosis. In the present case, such facts that there was no marked facial paresis and that the recovery of motor function started from peripheral portions of the upper extremity, coincide with the syndrome of occlusion of the rolandic veins, as described by Holmes et aL4 and Merwarth.; On the other hand, such facts that pain sensation was impaired and that the duration of flaccid palsy was fairly long, are not in accordance with the typical syndrome. It may be that the latter facts were relevant to a possible impairment of cerebral subcortical venous drainage due to formation of collateral venous channels from the cortex toward the subcortical structures. Observation of venous phase of carotid angiogram or of sinogram is the decisive means of diagnosing this disease. By this means, early and correct diagnosis of the disease will be possible, thus resulting in early treatment and good prognosis. REFERENCES 1 Dripps, R. D., Eckenhoff, J. E. and Vandam, L. D.: “Introduction to Anesthesia. The Principles of Safe Practice. 3rd Ed.” Philadelphia, W.B. Saunders Co., 1967, 529 pp. 2 Forbes, H. S. and Nason, G. I.: The cerebral
circulation: vascular responses to (A) hypertonic solutions and (B) withdrawal of cerebrospinal fluid, Arch Neurol Psychiat, 34: 533-547, 1935. 3 Gabrielsen, T. 0. and Heinz, E. R.: Spon-
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taneous aseptic thrombosis of the superior sagittal sinus and cerebral veins, Amer J Roentgenol, 107: 579-588, 1969. 4 Holmes, G . and Sargent, P.: Injuries of the superior longitudinal sinus, Brit Med J, 2: 493-498, 1915.
5 Merwarth, H. R.: Hemiplegia of cortical or venous origin (occlusion of rolandic veins), Brooklyn Hosp J , 2: 193-212, 1940. 0 Merwarth, H. R.: The syndrome of the rolandic vein (hemiplegia of venous origin), Amer J Surg, 56: 526-544, 1942.
Thrombosis of Rolandic Veins Following Lumbar Anesthesia: A Case Report Kazuki Sakata, M.D., Hiromu Yamada, M.D., Takeshi Chujo, M.D., Tatsuhiko Abe, M.D. and Juji Tsuchiya, M.D. Second Department of Surgery, G i f u University School of Medicine, G i f u
INTRODUCTION The syndrome of occlusion of the rolandic veins, unaccompanied by occlusion of the superior sagittal sinus, has been described by Menvarth5 and various later authors. However, occurrence of the syndrome following lumbar anesthesia seems to be quite rare. One such case, experienced by us, is reported. CASE REPORT
A 23-year-old female was admitted to our clinic on December 4, 1974, with chief complaints of convulsive attacks involving the right half of the body and paralysis of the right extremities. On November 21, or 13 days prior to admission, she noted right lower abdominal pain. Since the symptom did not improve, she consulted a surgeon and, being diagnosed as acute appendicitis, she underwent appendectomy under lumbar anesthesia on November 28. According to the surgeon her appendicitis was mild. Shortly after the operation she came to complain of severe headache, nuchal pain and nausea, which continued up to the time of admission to our clinic. On December 2, she noted motor disturbance of the right extremities and numbness sensation of the right half of Received for publication August 11, 1975,
the body. The motor disturbance was aggravated gradually, coming to show complete paralysis of the right extremities on December 3. In the next morning (the day of admission) an attack of clonic convulsion of the right leg, lasting for a few minutes, appeared, followed then by several attacks of tonic and clonic convulsions, involving the right half of the body and lasting for a few minutes at each time, on the same day. Consciousness was not impaired during the seizures. Her appetite was disturbed. Menstruation was regular and no oral contraceptive was used. She had no prior history of convulsion and her family’s medical history was nothing particular. On admission, her consciousness was clear. Systolic and diastolic blood pressures were 110 and 58 mmHg respectively. Severe left headache, especially in the occipital region, and neck stiffness were noted. Size of the pupils, light reflex, visual acuity and fundoscopic finding were all normal. Flaccid paralysis of the right extremities and slight weakness of the right facial muscles were noted. There was right sensory hemiparesis accompanied by paresthesia. Babinski reflex was positive on the right side. No abnormality was found in the abdomen except for a sutured appendectomy wound. Lumbar puncture, done on December 4, revealed that the cerebrospinal fluid (CSF) pressure was O m m of water, and the CSF,
356
K. Sakata
rt a/.
Thrombosis of Rolandic Veins
Fig. I (a and b): A-P view (a) and lateral view (b) of phlebogram. Arrows indicate sites of venous obstruction.
357
358
K. Sakata et al.
easily obtained by suction, was watery clear place in the following order: distal portions and showed no pleocytosis. Culture of CSF of the upper extremity, proximal portions was negative. thereof, distal portions of the lower extremity At the time of admission, bleeding time and proximal portions thereof. and coagulation time were normal, white cell On December 14 (10 days after admiscount was 4,800per cu.mm., red cell count sion), all the symptoms, including headache, was 330x lo4 per cu.mm., hematocrit was nuchal rigidity, sensory and motor disturb28% and platelet count was 3 4 ~ 1 0per~ ances of the right extremities and right posicu.mm. Serum protein was 8.2 mg/dl, and tive Babinski reflex, completely disappeared serum electrolyte and blood glucose levels and she was neurologically normal. She was were normal. discharged on December 17 and is continuEEG, recorded on December 5 , showed ing to be well subjectively and objectively diffuse moderate slowing and amplitude of five months after her discharge. Right carodiffuse 6 to 7 per second regular rhythms tid angiogram, done after her discharge, was was somewhat lower on the left side. No found to be normal. seizure discharge was noted. Left carotid angiogram, done on DecemDISCUSSION ber 6, revealed on phlebogram that the left rolandic veins were occluded near the porThe case presented here is a case of tion of their confluence to the superior sagit- thrombotic occlusion of the left rolandic tal sinus and collateral venous channels de- veins, which occurred four days after appenveloped (Fig. 1 a and b). In A-P view, the dectomy, done under lumbar anesthesia. Apleft side wall of the superior sagittal sinus pendicitis appeared to be mild and the opershowed some irregularities, suggesting pre- ation seemed to be uneventful, of course, sence of mural thrombi, but patency of the being unaccompanied by shock. Since no sinus was maintained sufficiently. Left serial marked fever was noted and there was no carotid angiogram, done on December 11, leucocytosis at the time of admission to our showed the same findings. clinic, a probability of infective cerebral Blood sedimentation rate, done on Decem- venous thrombosis, related to appendicitis, ber 7, was 16 mm in one hour and 43 mm in seems to be quite small. In view of the facts two hours. CSF pressure was found to be that headache, nuchal pain and nausea were recovered up to 65 mm of water on the same noted shortly after the operation and that the CSF pressure, measured on the day of day. After admission, she was treated by ad- admission, was 0 mm of water, it is certain ministration of anticonvulsant and hydro- that marked CSF hypotension following cortisone as well as intravenous infusion of lumbar puncture was present. It may be low molecular dextran solution. Convulsive reasonable to suppose that this CSF hypoattacks ceased on December 6. Toward that tension was etiologically related to thromtime, the formerly flaccid paralysis of the bosis of the rolandic veins. Dripps et a1.l describe headache, difficulright extremities became spastic, and voluntary movements of the extremities began to ties in hearing, ocular problems, traumatic recover. During the following several days, puncture and infection, as sequelae of lummotor palsy rapidly recovered and, simulta- bar puncture. They mention, further, that neously, right sensory hemiparesis disap- hypotension induced by lumbar anesthesia peared. The recovery of motor function took or hypoxemia due to respiratory failure may
Thrombosis of Rolandic Veins cause a reversible or irreversible impairment of the central nervous system, and that a central nervous system disorder may casually complicate, or a pre-existing such disorder may be aggravated by, lumbar anesthesia. They do not point out any possibility of occurrence of cerebral venous thrombosis, however. As far as we surveyed the literature, only one such case was found to be reported: i.e., Gabrielsen et al.“ reported a case of 40-yearold male case (their Case 4) who suffered from thrombosis of the superior sagittal sinus following appendectomy performed under lumbar anesthesia. No previous report has been found that occurrence of thrombosis circuinscribed to the rolandic veins following lumbar anesthesia, like in the present case, was observed. Relationship between CSF hypotension and cerebral venous thrombosis will next be discussed. It is generally known that the following factors contribute to formation of thrombosis: changes in blood properties, changes in vessel walls and slowing of blood flow. It is known that cerebral veins dilate as CSF pressure is reduced.’ Furthermore, it is considered that changes in relative position of the bridging veins interconnecting the cerebral surface and the superior sagittal sinus and consequent traction thereof, are important in causation of headache accompanying CSF hypoten~ion.~ Thus it is reasonable to suppose that the assumed retardation of blood flow within the dilated cerebral veins and/or retardation of blood flow within the portions of veins preceding the kinked or narrowed bridging veins, will facilitate thrombus formation. However, in view of rarity of cerebral venous thrombosis as a complication to CSF hypotension following lumbar puncture, its occurrence in the present case may be relevant to additive effects of other concomitant factors, such as anemia and dehydration
359
due to anorexia consequent on appendicitis and subsequent CSF hypotension. Anyhow, it is to be pointed out that, in case some symptom of central nervous system lesions occur following lumbar anesthesia, there certainly is a small probability, besides probabilities of sequelae of hypotension or hypoxemia during anesthesia, that the symptoms may be due to cerebral venous thrombosis. In the present case, such facts that there was no marked facial paresis and that the recovery of motor function started from peripheral portions of the upper extremity, coincide with the syndrome of occlusion of the rolandic veins, as described by Holmes et aL4 and Merwarth.; On the other hand, such facts that pain sensation was impaired and that the duration of flaccid palsy was fairly long, are not in accordance with the typical syndrome. It may be that the latter facts were relevant to a possible impairment of cerebral subcortical venous drainage due to formation of collateral venous channels from the cortex toward the subcortical structures. Observation of venous phase of carotid angiogram or of sinogram is the decisive means of diagnosing this disease. By this means, early and correct diagnosis of the disease will be possible, thus resulting in early treatment and good prognosis. REFERENCES 1 Dripps, R. D., Eckenhoff, J. E. and Vandam, L. D.: “Introduction to Anesthesia. The Principles of Safe Practice. 3rd Ed.” Philadelphia, W.B. Saunders Co., 1967, 529 pp. 2 Forbes, H. S. and Nason, G. I.: The cerebral
circulation: vascular responses to (A) hypertonic solutions and (B) withdrawal of cerebrospinal fluid, Arch Neurol Psychiat, 34: 533-547, 1935. 3 Gabrielsen, T. 0. and Heinz, E. R.: Spon-
360
K. Sakata et al.
taneous aseptic thrombosis of the superior sagittal sinus and cerebral veins, Amer J Roentgenol, 107: 579-588, 1969. 4 Holmes, G . and Sargent, P.: Injuries of the superior longitudinal sinus, Brit Med J, 2: 493-498, 1915.
5 Merwarth, H. R.: Hemiplegia of cortical or venous origin (occlusion of rolandic veins), Brooklyn Hosp J , 2: 193-212, 1940. 0 Merwarth, H. R.: The syndrome of the rolandic vein (hemiplegia of venous origin), Amer J Surg, 56: 526-544, 1942.
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