involvement of cerebral functions in acute carbon monoxide poisoning with special reference to...

Folia Psychiatrica et Neurologica Japonica, Vol. 21, No. 3, 1967

INVOLVEMENT OF CEREBRAL FUNCTIONS IN ACUTE CARBON MONOXIDE POISONING WITH SPECIAL

REFERENCE TO OCCIPITAL LOBE FUNCTIONS

Yoshigoro KUROIWA, M.D., Kenshiro SHIDA, M.D., Keiji NAGAMATSU, M.D., Motohiro KATO, M.D. and Tetsuji SANTA, M.D.

Department of Nerirology, Neurologicul Institrite, Fctciilty of Medicine, Kyirshri University (Frrkuoka, Japan J

INTRODUCTION

The pattern of cerebral involvement in acute carbon monoxide (CO) intoxication has been reported to involve the globus pallidus, and the parietal, temporal, and occipital lobes with the clinical manifestations of parkinsonism, amnesia, and an apraxia- agnosia syndrome') ,2).5) # 7 ) ~ 3 ) ~ 6 ) ~ 7 ) ~ 1 8 ) . However, most of these reports have been made on sporadiqcases. We had the opportunity to examine a group of patients with CO poisoning resulting from a large scale gas explosion in Y-coal mine in Japan in 1965. The purpose of this paper is to report on the clinical features of CO poisoning in these patients in order to stress the occipital lobe dysfunction.

MATERIAL

The gas explosion of Y-coal mine in Fukuoka, Japan, occurred on June 1, 1965, at 0:30 P.M., ith production of a considerable amount of CO gas. The concentra- tion of CO in the air of the mine was 0.5 per cent one hour after the explosion, and below 0.01 per cent after two hours. At the time of the explosion 552 men were working underground. 237 were found dead, and 315 were rescued alive (Table 1 ) . Most of the dead cases had red skin without evidence of trauma or external burns. A clinical diagnosis of CO intoxication as cause of death was made. Of the 315 rescued, 25 were admitted immediaely to the local coal mine hospital because of un conscious-

Table 1. Casualities in Y-Coal Mine Explosion (June 1, 1965, Fukuoka, Japan)

Miners Exposed to Carbon Monoxide 552 100% Dead 237 43 % Alive 315 57%

Not Hospitalized 290 52% Hospitalized 25 5%

Received for publication, Sept. 9, 1967

190 Y. Kuroiwa, K. Shida, K. Nagamatsu, M. Kato and T. Santa

5

6

7

8

ness, weakness or other complaints. A few of them had injuries or burns. Seven of 1 I cases tested qualitatively for blood CO within two days were positive. A summary of the 25 cases in shown in Table 2. Of the 25, four severely affected patients (Table 2) were transfered to the Kyushu University Hospital ( K U H ) . This communication will describe these 4 cases.

Table 2. Summary of Patients Admitted to Local Hospital

transcient amnesia, confusion 36 (not clear) inative N., K.

T., K. 21 M 3 hrs. confusion, amnesia

hyperactive DTR, weakness of rt. leg T., T. 37 M 7 hrs.

M., Y. 40M 4-5 hrs. none

~- ~

case N ~ . 1 N~~~ I ! Duration of Symptoms During First Age' Sex unconsciousness ~ hospital days

T., M.

H., J .

M., B.

9 other cases

amnesia, disorient. visual agnosia 1 I N., K. 1 4 6 M 1 7hrs.

~ _ _ _ _ _ ~

41 M within 1 hr. none

41 M 10 min. none

34 M 10 min. ? none

none

amnesia, disorient. visual dist., irritation

confus.ion, visual dist. amnesia N., N. ~ 31 M 1 7hrs.

1 I I I I

4 I F., N. 1 39 M 1 8hrs. amnesia, visual impairment

9 1 Y . , I. I 47 M 1 3-4hrs. 1 knee jerk hyperactive I 10 I M., A. 1 42 M 1 3-4hrs. I none 1 1 1 E., M. 37 M within 3 hrs.

12 1 I., T. 1 36 M I 4hrs.

13 1 A., S. 1 3 9 M 1 2hrs. 1 none I 14

15

16

17-25

OBSERVATION

Case 1 . N., K. 46 year old man When he was rescued at 8 P.M., 7% hours after the explosion, he appeared un-

responsive to various stimuli. The next day he began to respond t o verbal stimuli, but was markedly disoriented. He had severe amnesia, poor vocabulary, and complained of blurred vision. That day, he was

H e opened his eyes but was akinetic and mute.

Carbon Monoxide Poisoning and the Occipital Lobe Functions 191

transfered to KUH. The neurlogical findings on admission were:

although inactive and emotionally apathetic. 1 .

2. 3. 4. 5. Intact sensations. 6.

1.

Confusion and disorientation to time, place and person; conscious and alert

Fluctuating visual acuity with a suggestion of visual object agnosia. Absence of other cranial nerve signs. Normal tone, strength, and reflexes in limbs.

Except for slightly stiff neck, no extra-pyramidal or cerebellar signs. The symptoms and signs after one week were:

Memory-He could remember his name and birthdate and the names of his wife and brother. He had no memory of the accident or of incidents occuring after return of consciousness. He forgot test items within a few minutes. Thus there was loss of recent meomry but not of remote memory.

2. Visual Agnosia-A) Identification: He could visually recognize and name some common objects like a knife, a watch and a pen, but others were recognized only by touch. He could not recognize pictures of figures drawn on paper, nor could he identify items in a composite picture. There was no finger agnosia or right-left disorientation (i.e. no Gerstmann syndrome). He could not recognize his wife or his brother. When asked who this man (his brother) was, he replied that it was a nurse or an attendant. When he heard the voice, he could say it was his brother. B) Inter- pretation: He could not rend letters or words in either kanji (Chinese ideograms) or kana (Japanese phonograms), but he could recognize letters written on his skin or which he had traced out (visual alexia). He showed considerable difficulty with mental calculations. This difficulty with calculations was even more pronounced when done on paper, because of the visual agnosia.

Fig. 1. Drawing test in case 1. The left drawings are spontaneous writing of a house and a man. The right ones are copies of a geometrical figure and a house. Note the greater clumsiness in copying than in spontaneous writing as well as the spatial disorientation.

192 Y. Kuroiwa. K. Shida, K. Nagamatsu, M. Kato and T. Santa

3. Skills-Writing was difficult, with clumsiness in pictures and letters and evidence of constructional apraxia. Spontaneous writing was better than copying (Fig. 1). Copying of pictures showed the “closing-in” phenomenon of Mayer-Gross and signs of visual-spatial disorientation. Construction with blocks and making shapes with his fingers (autotopokinesis) was poorly done. He could not place the names of familiar large cities on a map, nor could he return from the toilet to his hospital bed even after numerous instructions.

4. Aphasia-There was no difficulty in finding words (amnestic aphasia), no difficulty in speech (motor aphasia), and no other sign of aphasia.

Course: He was treated with “hyperbaric oxygen” (2280 mm Hg-100% 0,) 2 hours a day for 10 days starting the 2nd day. He gradually improved. After three months only slight visual impairment was present, and most of these agnosia-apraxia had disappeared.

Case 2 S., H. 42 year old man He awoke in the tunnel and complained im-

mediately of visual loss He was rescue d8 hours after the accident and was hospitalized immediately. He was very confused, talkative, and euphoric. The next morning he was disoriented for time and place. Vision was markedly impaired. He could recognize his friends by their voices, but not by sight. He was transfered to KUH on the second day

On admission, he appeared physically normal. No paralysis, no trauma, and no burns were seen. He was conscious, but markedly disoriented. He could recognize the hospital, but did not know the name of thg fiaspital. He had amnesia for recent events.

He complained that things appeared double or triple (polyopsia), and distorted in shape (metamorphopsia). On the 3rd hospital day he complained of seeing hor- rible colors (kakopsia). He could recognize many objects on sight, but sometimes had to feel them in order to identify them. He could not recognize simple pictures of common objects or geometrical figures, nor name objects in pictures of objects over- lapping in various combinations.

Writing of letters was good, but picture drawing was clumsy. Copying was more clumsy than spontaneous drawing, a sign of visual disorientation. He had some impairment in ability to do arithmetic. Visual acuity fluctuated from day to day, and showed marked fatigability. He had geographical disorientation, and here was constructional apraxia with block tests or in drawing. Neither finger agnosia, nor right-left disorientation were seen.

Emotional state, visual recognition and polyopsia improved after three weeks. Metamorphopsia had disappeared.

After 6months he had made quite a good recovery.

He was unconscious for 5 hours.

Recognition of colors was good. He could read sentences, but sometimes with difficulty.

Course:

Case 3. N., N. 37 year old man He remembered the time of explosion, but was then unconscious for about 6 hours.

He was rescued 7% hours after the explosion, excited, disoriented and talkative. Vision seemed to be impaired. Headache was present and was somewhat somnolent for three days.

After 7 days he was transfered to KUH. At that time he was alert and oriented.


Memory and calculation ability were good. His chief complaint was visual impairment. The visual acuity was 0.1 (right) and 0.04 (left) on teh eleventh day. No change in optic fundi was seen. There was a bilateral paracentral scotoma in the left lower quadrant (Fig. 2 ) . Other cranial nerves, motor and sensory functions, and coordination were practically normal. Additional Visual symptoms were:

He had no double vision.

N.N. S40 - 6- 12. 1 R

Fig. 2. Visual field defect in case 3. Black area : absolute scotoma. Shaded area : relative scotoma.

1, Prolonged gaze caused blurring. 2. Recognition and naming of simple geometrical figures of pictures of objects

( a square, a star, a circle, a house, a desk, a pencil) were correct with a few excep- tions (a chair, shoes). Explanation of pictures was not possible. Poppelreuter’s composite pictures could not be understood.

Reading letters or sentences was difficult, but was improved by tracing with fingers (slight visual-agnostic alexia) .

Writing letters, figures and copying were good. Naming of colors was good.

3.

4. 5. 6. Constructional apraxia was present. Autotopokinesis for fingers was slightly

impaired. Course: There was transient rigidity and hyperreflexia in the legs about 2-3 week

after the poisoning. Vision improved after 3 months to 1.2 ( r . ) and 0.7 ( l . ) , but he complained of fatigability in reading. After 3 months most of the symptoms had improved except for slight visual impairment and slight reading diffifficulty.

Case 4. F., N. 39 year old man He was unconscious for about 8 hours and admitted to the hospital immediately.

He was confused, amnesic for recent events, and visually impaired and disoriented. He was transfered to KUH on the next day. The main findings on admission were: euphoria, irritability and disorientation for time and place.


Case 1 Case 2 Case 3 Case 4

Disorientation Emotional change Amnesia

Agnosia- Apraxia Visual impairment

- - Rigidity f

H yperreflexia I + I * I -

+ + + + + + + + tt tt + + tt + + + i t + + +

Table 4. Agnosia and Apraxia

I Case 1 I Case 2 1 Case 3 I Case 4

-

+ st +

Metamorphopsia Object agnosia (visual) Alexia (visual) Visuospatial agnosia

+ + + * f + + +

f +

-

-

Constructional apraxia + * * Autotopakinesis I + I + Gerstmann’s syndrome - - - -

Aphasia 1 - 1 - 1 - 1 -


even in late stages. Distortion of shape or color was frequent. Higher visual per- ceptional disorders included object agnosia, pictorial agnosia, alexia, etc., all probably fundamentally related to the object agnosia.

DISCUSSION

The clinical manifestations of CO-encephalopathies seen after the explosion of Y-coal mine. Fukuoka, Japan, have been presented. Thi sexplosion caused 237 deaths and 25 casualties due to CO intoxication. The four most severe cases were carefully examined, and are reported here. The incidence of permanent neurologic deficits in acute CO poisoningjs said to be very low, 0.05-0.20% (Shillito et a115)). In the Y-coal mine accident 4 patients had severe neurological sequelae, about I per cent of the rescued.

There have been many recent Japanese reports on neuropsychiatric aspects4ab,6,*.lo,ll,14.19.) of acute CO poisoning. The cases reported here presented with unconsciousness and subsequently showed disorientation, visual perceptual changes and amnesia. Neurological and mental changes that can be attributed to focal lesions were seen. The rarity of neurological signs sug- gesting Parkinsonism is a noteworthy feature, as is the frequent occurrence of agnosia and apraxia. Constructional apraxia was one of the commonest features, seen both in writing and in the block test. Apraxia with fingers (autotopokinesis) was also seen very often. None of the four showed aphasic disturbance, although it has been re- ported12). Speech was generally fluent and verbose. These findings suggest that cortical damage was not as prominent in the frontal regions.

The commonest cortical symptonis arose in the occipital or parieto-temporal lobes. Blurred vision (cerebral asthenopia) , metamorphopsia, related visual percep- tional changes and visual agnostic syndromes were common. There was elementary visual impairment with fluctuating visual acuity, and in some cases central scotomata. Difficulty in recognizing objects, figures, pictures and letters by sight indicated visual agnosia, while normal ability to recognize by touch indicated absence of tactile agnosia. Attempts at reading demonstrated alexia. Color perception was generally correct. There was no evidence of Gerstmann syndrome, while in the Mike accident 8 out of 44 severe cases showed this syndromelo).

Visuo-spatial disabilities were manifest as a marked disturbance in drawning of figures and pictures. The “closing-in’’ phenomenon was seen in the early stages. Ability to count objects seen was normal (no Baht ’s syndrome). Topographical disturbances may have been partially due to general intellectual damage.

As Critchleys) pointed out, the classical dichotomy of vision into higher and lower levels of functional activity or into primary and secondary phases of recognition is probably not valid. These patients had a continuous impairment from the primary to the higher functions of visual perception. Although CO intoxication is a diffuse process, the same basic pathogenesis for all these visual impairments can be assumed-namely, the greater vulnerability of the occipital cortex. The photic evoked potential showed marked diminution in the occipital lobes, especially in the secondary responses. This suggests the relative vulnerability of the occipital integrating func- tiongJ1). Additional cases now being prepared for publication, support the contention that anoxia is the major cause of the occipital lobe syndrome.


SUMMARY

The neuropsychiatric manifestations of CO intoxications at the Y-coal mine explosion at Fukuoka, Japan, occurring in 1965 were reported utilizing the four most severe cases.

I . All four cases showed unconsciousness for several hours, followed by disorientation, emotional changes, and marked impairment of recent memory.

2. All cases showed visual impairment of both, elementary and higher visual perception: decreased vision, central scotoma, metamorphopsia, kalopsia, kakopsia, polyopsia and visual agnosias (visual object agnosia, visual figure agnosia, pros- opagnosia, alexia and visual spatial agnosia).

3. Letter writing and picture drawing also demonstrated the visual agnosia. 4. Constructional apraxia and impairment of autotopokinesis were common. 5. None of patients had Gerstmann’s syndrome or aphasia. 6. Extrapyramidal or pyramidal manifestations were not prominent. All these

findings suggest a particular vulnerability of the occipital lobe to CO intoxication.

REFERENCES

Ajuriaguerra, J. Zazzo, R. & Granjon, N.: Le phenomene d‘accolement au modelf (closing-in) dans un syndrome d’apraxie oxycarbonee. L’encephale, 38( 1 ) : 1-20, 1949. Akimoto, H.: Uber die Apraxie im besonderen Zusammenhang mit der optischraumli- chen Agnosie. Psychiat. Neurol. Jap. 35(4) : 267-306, 1932. Critchley, M.: The Problem of visual agnosia. J. Neurol. Sci. 1: 274-290, 1964. a ) Fujii, M.: The Histopathology of the central nervous system lesions caused by

carbon monoxide poisoning. A reporf of ten cases with an acute and protracted clinical course. Psychiatr. Neurol. Jap. 62: 1-34, 1960.

h ) Fujii, M., Moriya, A. & Yamabe, A.: The carbon monoxide poisoning especially of the delayed cases. Recent. Adv. Neurol .Sci. (Jap.) 4: 67-82, 1959.

Hama, To.: Constructional apraxia. Jikeika Medical Journal 71( 1 ) : 98-1 18, 1956. Iizuka, R., Nishioka, N. and Furuya, 0.: Ein Beitrag zur akuten CO-introxication. Recent Adv. Neurol. Sci. (Jap.) 9: 71-75, 1965. Isakower, 0. and Schilder, P.: Optische-raumliche Agnosie und Agraphie. Z. ges. Neurol. Psychiat. 113: 102-142, 1928. Katsuki, S.: Neuropsychiatric symptoms of carbon-monoxide intoxication seen in the coal mine explosion (Jap.) Jap. J. Clin. Med. 23: 1928-1936, 1965. Kuroiwa, Y., Umezaki, H., Katsuki, S. and Kawagoe, H.: Flat EEG in acute CO intoxication. Proc. Japan EEG SOC. 13th Congress, p. 114-116, 1964. Kuroiwa, Y., Miyazaki, T., Umezaki, H., Kato, M., Santa, T., Sakurai, T., Nishizono, M., Takamatsu, I., Yukitake, R., Katsuki, S., Kawagoe, H., Nagamatsu, K., Okayama, M., Iwasawa, A., and Higashi. Y.: Symptoms of acute stage in a group of cases with CO intoxication. Psychiatr. Neurol. Jap. 66: 246, 1964. Kuroiwa, Y.: The carbon monoxide poisoning, Jap. J. Clin. Med. 25(8): 1647-1652, 1967. Miyake, K. & Hashimoto, K. : Die psychischen Storungen nach acuter Kohlenoxyd- vergiftung. Psychiatrica et neurologia japonica, 15(6) : 265-280, 1916. Ohashi, H. & Satio, H.: Agnosie spatiable unilateralesus un cas d’intoxication a I’oxyde de carbon. Psychiat. Neurol. Jap. 61(9): 1167-1 174,, 1959. Omaru, I., Inanaga, K., Akimoto, T., Nakamura, K., Yamamoto, Y., Hirose, A., To-


risu, M., Ogata, M., Yamaguchi, E., Honma, S. & Shirakawa, Y.: Psychiatric and neurologic symptoms of carbon monoxide intoxication. Psychiatr. Neurol. Jap. 66 : 247, 1964.

IS) Shillito, F. H., Drinker, C. K., & Shaughnessy, T. J.: The problem of nervous and mental sequelae in carbon monoxide poisoning. JAMA 106: 669-674, 1936.

16) Solomon, A. P.: Acalculia, other agnosia and multiple neuritis following carbon monoxide poisoning. Med. Clin. North. Amer. 16: 531-1932.

17) Steele, G.D.E. & Hegarty, A. B.: Parieto-occipital syndrome following carbon monoxide poisoning. J. Med. Sci. 96: 1015-1023, 1950.

1 8 ) Sterz,: Amnestische Apraxie bei Kohlenoxydgasvergiftung. Z. ges. Neurol. Psychiat.

19) Tatetsu, M., Kiyota, K., Toya, G., Teraoka, H., Fujita, E., Yamagata, M., Inoue, Na- kamura, E., Takagi, M., Harada, M., Mimura, K., Kozuma, y., Kozuma, y . , Miya- kawa, Y., Tornonari, H., Murayama, E., Kinoshita, H., Yasuoka, F., Sumiyoshi, S., Miyoshi, K., Miyakawa, M., Nakashima, A., Higashi, K., & Nishi, K.: Psychiatric and neurologic studies of acute carbon monoxide intoxication occurred as a group. Psychiatr. Neurol. Jap. 66: 246, 1964.

24: 177-181, 1921.

involvement of cerebral functions in acute carbon monoxide poisoning with special reference to...

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