Re: Matt--meningitis-encephalitis

[Guest guest]

Matt,

It sounds like she's gotten alot worse with the Cellcept? Sounds like this drug is not her magic bullet. Her M.D.'s "this is to be expected" is bull. She shouldn't be getting worse if the meds the right one. Rarely does sarc progress this quickly- have they done a spinal tap to make sure she doesn't have some meningitis-encephalitis going on?

Darlene is right you need second opinions on this-- they are missing something.

Here is an article that was written in 1964--

1576 19 DecAber 1964

Medical Memoranda

Acute Sarcoid Meningo-encephalitis

Brit. mAd. _., 1964, 2, 1576

Meningo-encephalitis is a rare complication of sarcoidosis. The

onset may be abrupt and deterioration rapid. Failure to be

aware of this may result in the death of a patient with a treatable

condition.

CASE REPORT

A woman aged 42 was admitted to hospital on 22 January 1963

having had several generalized convulsions early that morning.

There was no family history of epilepsy. The only information

available on admission was that

her weight had fallen by 35 kg.

in two years and that she had

been drowsy the previous day.

She was drowsy, disorientated,

and incontinent of

_| | 9- urine and faeces. Though her

neck was stiff, Kernig's sign

was not present. Both plantar

responses were extensor.

Examination of sensory nerve

function was unreliable on

account of lack of co-operation,

but subsequent examinations

did not reveal any

sensory loss.- The optic fundi

were normal and there were no

cranial nerve lesions.-

There were numerous purple

areas of skin infiltration

which were raised, irregular in

outline, and varied from 1 to

6 cm. in greatest diameter.

They were confined to the face,

back of the chest, and arms,

particularly the upper arms;

the lesions tended to be symmetrical.

There were two

subcutaneous nodules without

associated skin infiltration, one

on the left forearm and the

other on the anterior abdominal

wall.

Large, rubbery, and discrete

lymph nodes were palpable in

the neck, supraclavicular

fossae., axillae, epitrochlear

Cystic and destructive changes in the regions, and groins. The left

phalanges, January 1963. little finger and the right

middle finger were swollen.

The liver and spleen were not palpable. Her temperature was

normal. The chest radiograph was normal, but films of the

hands revealed destructive changes (see Fig.).

The lumbar cerebrospinal fluid contained 8 lymphocytes/c.mm.,

protein 250 mg./100 ml., sugar 18 mg./100 ml., and chloride 730

mEq/l. The Wassermann reaction was negative. The results of

other investigations were haemoglobin 14.7 g./100 ml., erythrocyte

sedimentabtin rate 32 mm. in one hour (Wintrobe), and total serum

proteins 5.2 g./100 ml., of which 2.4 g. was albumin and 2.8 g.

globulin (0.3 g., 0.7 g., 0.7 g., and 1.2 g.). The serum calcium was

8.6 mg./100 ml., inorganic phosphate 3.6 mg./100 ml., and alkaline

phosphatase 8.3 King-Armstrong units/100 ml.

She became progressively more drowsy and had infrequent generalized

convulsions. Biopsy of an epitrochlear node and an area of

skin infiltration was performed on 25 January. Since her general

condition was deteriorating rapidly and sarcoidosis was the only

treatable condition compatible with the signs, she was given prednisone

40 mg. daily while the result of the biopsy was awaited. There

was a dramatic improvement in her mental and physical condition

within 48 hours. The histological features of both gland and skin

infiltration were those of sarcoidosis. The prednisone was reduced

over four weeks to a maintenance dose of 10 mg. daily, which was

further reduced to 5 mg. in May 1963.

When she was readmitted in May 1963 for reassessment the skin

infiltrations were contracted, wrinkled, and depressed, and were a

greyish purple colour. No lymph nodes were palpable. The subcutaneous

nodule on the abdominal wall had disappeared and the

nodule on the left forearm was much smaller. The swelling of the

fingers had subsided and a radiograph showed that recalcification

of the phalanges had begun. The only neurological abnormality

was that the plantar responses were extensor.

The cerebrospinal fluid was now normal: there was 1 lymphocyte/

c.mm., protein 40 mg./100 ml., sugar 49 mg./100 ml., and chloride

710 mEq/l. The erythrocyte sedimentation rate was 35 mm.

In August 1963 the E.S.R. had fallen to 30 mm. in one hour.

The total serum protein was 6.5 g./100 ml., of which 3.35 g. was

albumin and 3.15 g. globulin; the electrophoretic pattern was

normal.

COMMENT

The response to treatment with adrenal corticosteroids in

patients with sarcoidosis of the central nervous system is unpredictable

and is often disappointing. The signs and

symptoms may diminish spontaneously without treatment.

This patient was critically ill before treatment, the clinical

response was dramatic, and the cerebrospinal fluid returned to

normal. A similar response to treatment with adrenal corticosteroids

was obtained in the only other case of acute sarcoid

meningo-encephalitis that is recorded as having been treated

in this way (Carstensen and Norviit 1953).

Neurological signs may develop when there is no evidence of

sarcoid elsewhere, though six of seven patients described by

(1961) had at one time had demonstrable pulmonary

involvement, which in one case was apparent only in a chest

radiograph taken 10 years earlier.

Sarcoidosis should always be considered in the differential

diagnosis of a patient with meningo-encephalitis, because the

response to treatment with adrenal corticosteroids is excellent.

I am grateful to Dr. W. D. Brinton for permission to report his

case.

PETER RICHARDS, M.A., M.B., M.R.C.P.

-St. 's Hospital, London.

REFERENCES

Carstensen, B., and Norviit, L. (1953). Nord. Med., 49, 299.

, A. G. (1961). Postgrad. med. Y., 37, 431.

To: neurosarcoidosis Sent: Tue, January 19, 2010 6:24:07 PMSubject: Off Line

Finally getting back into reading posts. I apologize for being remiss on birthdays and saying hello. Been a rough patch here with , After a weekend trip to my brothers she came home weak & disoriented. At first I thought it was just being over tired, but now it seems to be more than that. Lately trips away from home are taking a tremendous toll on her. I am finding that her speech patterns are really bad and so is her mobility. Doctors say it is to be expected, but I keep asking why if the meds are supposedly working? Sorry I am venting, but does anyone have any suggestions regard to this. Thanks matt

[Guest guest]

Thanks. I was back on the phone with them today. I am now awaiting additional info & getting impatient. did have a spinal tap last year I believe and there was no meningitis etc. That does not mean that something else is not going on. Thanks. Time for me to yell a bit louder so they hear me. MattSubject: Re: Matt--meningitis-encephalitisTo: Neurosarcoidosis Date: Wednesday, January 20, 2010, 10:36 AM

Matt,

It sounds like she's gotten alot worse with the Cellcept? Sounds like this drug is not her magic bullet. Her M.D.'s "this is to be expected" is bull. She shouldn't be getting worse if the meds the right one. Rarely does sarc progress this quickly- have they done a spinal tap to make sure she doesn't have some meningitis-encephal itis going on?

Darlene is right you need second opinions on this-- they are missing something.

Here is an article that was written in 1964--

1576 19 DecAber 1964

Medical Memoranda

Acute Sarcoid Meningo-encephaliti s

Brit. mAd. _., 1964, 2, 1576

Meningo-encephaliti s is a rare complication of sarcoidosis. The

onset may be abrupt and deterioration rapid. Failure to be

aware of this may result in the death of a patient with a treatable

condition.

CASE REPORT

A woman aged 42 was admitted to hospital on 22 January 1963

having had several generalized convulsions early that morning.

There was no family history of epilepsy. The only information

available on admission was that

her weight had fallen by 35 kg.

in two years and that she had

been drowsy the previous day.

She was drowsy, disorientated,

and incontinent of

_| | 9- urine and faeces. Though her

neck was stiff, Kernig's sign

was not present. Both plantar

responses were extensor.

Examination of sensory nerve

function was unreliable on

account of lack of co-operation,

but subsequent examinations

did not reveal any

sensory loss.- The optic fundi

were normal and there were no

cranial nerve lesions.-

There were numerous purple

areas of skin infiltration

which were raised, irregular in

outline, and varied from 1 to

6 cm. in greatest diameter.

They were confined to the face,

back of the chest, and arms,

particularly the upper arms;

the lesions tended to be symmetrical.

There were two

subcutaneous nodules without

associated skin infiltration, one

on the left forearm and the

other on the anterior abdominal

wall.

Large, rubbery, and discrete

lymph nodes were palpable in

the neck, supraclavicular

fossae., axillae, epitrochlear

Cystic and destructive changes in the regions, and groins. The left

phalanges, January 1963. little finger and the right

middle finger were swollen.

The liver and spleen were not palpable. Her temperature was

normal. The chest radiograph was normal, but films of the

hands revealed destructive changes (see Fig.).

The lumbar cerebrospinal fluid contained 8 lymphocytes/ c.mm.,

protein 250 mg./100 ml., sugar 18 mg./100 ml., and chloride 730

mEq/l. The Wassermann reaction was negative. The results of

other investigations were haemoglobin 14.7 g./100 ml., erythrocyte

sedimentabtin rate 32 mm. in one hour (Wintrobe), and total serum

proteins 5.2 g./100 ml., of which 2.4 g. was albumin and 2.8 g.

globulin (0.3 g., 0.7 g., 0.7 g., and 1.2 g.). The serum calcium was

8.6 mg./100 ml., inorganic phosphate 3.6 mg./100 ml., and alkaline

phosphatase 8.3 King-Armstrong units/100 ml.

She became progressively more drowsy and had infrequent generalized

convulsions. Biopsy of an epitrochlear node and an area of

skin infiltration was performed on 25 January. Since her general

condition was deteriorating rapidly and sarcoidosis was the only

treatable condition compatible with the signs, she was given prednisone

40 mg. daily while the result of the biopsy was awaited. There

was a dramatic improvement in her mental and physical condition

within 48 hours. The histological features of both gland and skin

infiltration were those of sarcoidosis. The prednisone was reduced

over four weeks to a maintenance dose of 10 mg. daily, which was

further reduced to 5 mg. in May 1963.

When she was readmitted in May 1963 for reassessment the skin

infiltrations were contracted, wrinkled, and depressed, and were a

greyish purple colour. No lymph nodes were palpable. The subcutaneous

nodule on the abdominal wall had disappeared and the

nodule on the left forearm was much smaller. The swelling of the

fingers had subsided and a radiograph showed that recalcification

of the phalanges had begun. The only neurological abnormality

was that the plantar responses were extensor.

The cerebrospinal fluid was now normal: there was 1 lymphocyte/

c.mm., protein 40 mg./100 ml., sugar 49 mg./100 ml., and chloride

710 mEq/l. The erythrocyte sedimentation rate was 35 mm.

In August 1963 the E.S.R. had fallen to 30 mm. in one hour.

The total serum protein was 6.5 g./100 ml., of which 3.35 g. was

albumin and 3.15 g. globulin; the electrophoretic pattern was

normal.

COMMENT

The response to treatment with adrenal corticosteroids in

patients with sarcoidosis of the central nervous system is unpredictable

and is often disappointing. The signs and

symptoms may diminish spontaneously without treatment.

This patient was critically ill before treatment, the clinical

response was dramatic, and the cerebrospinal fluid returned to

normal. A similar response to treatment with adrenal corticosteroids

was obtained in the only other case of acute sarcoid

meningo-encephaliti s that is recorded as having been treated

in this way (Carstensen and Norviit 1953).

Neurological signs may develop when there is no evidence of

sarcoid elsewhere, though six of seven patients described by

(1961) had at one time had demonstrable pulmonary

involvement, which in one case was apparent only in a chest

radiograph taken 10 years earlier.

Sarcoidosis should always be considered in the differential

diagnosis of a patient with meningo-encephaliti s, because the

response to treatment with adrenal corticosteroids is excellent.

I am grateful to Dr. W. D. Brinton for permission to report his

case.

PETER RICHARDS, M.A., M.B., M.R.C.P.

-St. 's Hospital, London.

REFERENCES

Carstensen, B., and Norviit, L. (1953). Nord. Med., 49, 299.

, A. G. (1961). Postgrad. med. Y., 37, 431.

From: D. <dmatt1960 (AT) yahoo (DOT) com>To: neurosarcoidosis@ yahoogroups. comSent: Tue, January 19, 2010 6:24:07 PMSubject: Off Line

Finally getting back into reading posts. I apologize for being remiss on birthdays and saying hello. Been a rough patch here with , After a weekend trip to my brothers she came home weak & disoriented. At first I thought it was just being over tired, but now it seems to be more than that. Lately trips away from home are taking a tremendous toll on her. I am finding that her speech patterns are really bad and so is her mobility. Doctors say it is to be expected, but I keep asking why if the meds are supposedly working? Sorry I am venting, but does anyone have any suggestions regard to this. Thanks matt

[Guest guest]

MATT I MISSED SEEING YOUR INPUT ON LINE.I WAS GLAD TO SEE YOU POST YESTERDAY.I PRAY THAT YOUR WIFE START TO FEELING BETTER.CONTINUE TO CARE FOR HER AND LOVE HER.I PRAY THAT GOD WILL GRANT YOU THE STRENGTH,KNOWLEDGE,CARE,LOVE AND THE REST THAT YOU NEED.STAY BLESSED.HELENFrom: tracie feldhaus <tiodaat2001@

yahoo.com>Subject: Re: Matt--meningitis- encephalitisTo: Neurosarcoidosis@ yahoogroups. comDate: Wednesday, January 20, 2010, 10:36 AM

Matt,

It sounds like she's gotten alot worse with the Cellcept? Sounds like this drug is not her magic bullet. Her M.D.'s "this is to be expected" is bull. She shouldn't be getting worse if the meds the right one. Rarely does sarc progress this quickly- have they done a spinal tap to make sure she doesn't have some meningitis-encephal itis going on?

Darlene is right you need second opinions on this-- they are missing something.

Here is an article that was written in 1964--

1576 19 DecAber 1964

Medical Memoranda

Acute Sarcoid Meningo-encephaliti s

Brit. mAd. _., 1964, 2, 1576

Meningo-encephaliti s is a rare complication of sarcoidosis. The

onset may be abrupt and deterioration rapid. Failure to be

aware of this may result in the death of a patient with a treatable

condition.

CASE REPORT

A woman aged 42 was admitted to hospital on 22 January 1963

having had several generalized convulsions early that morning.

There was no family history of epilepsy. The only information

available on admission was that

her weight had fallen by 35 kg.

in two years and that she had

been drowsy the previous day.

She was drowsy, disorientated,

and incontinent of

_| | 9- urine and faeces. Though her

neck was stiff, Kernig's sign

was not present. Both plantar

responses were extensor.

Examination of sensory nerve

function was unreliable on

account of lack of co-operation,

but subsequent examinations

did not reveal any

sensory loss.- The optic fundi

were normal and there were no

cranial nerve lesions.-

There were numerous purple

areas of skin infiltration

which were raised, irregular in

outline, and varied from 1 to

6 cm. in greatest diameter.

They were confined to the face,

back of the chest, and arms,

particularly the upper arms;

the lesions tended to be symmetrical.

There were two

subcutaneous nodules without

associated skin infiltration, one

on the left forearm and the

other on the anterior abdominal

wall.

Large, rubbery, and discrete

lymph nodes were palpable in

the neck, supraclavicular

fossae., axillae, epitrochlear

Cystic and destructive changes in the regions, and groins. The left

phalanges, January 1963. little finger and the right

middle finger were swollen.

The liver and spleen were not palpable. Her temperature was

normal. The chest radiograph was normal, but films of the

hands revealed destructive changes (see Fig.).

The lumbar cerebrospinal fluid contained 8 lymphocytes/ c.mm.,

protein 250 mg./100 ml., sugar 18 mg./100 ml., and chloride 730

mEq/l. The Wassermann reaction was negative. The results of

other investigations were haemoglobin 14.7 g./100 ml., erythrocyte

sedimentabtin rate 32 mm. in one hour (Wintrobe), and total serum

proteins 5.2 g./100 ml., of which 2.4 g. was albumin and 2.8 g.

globulin (0.3 g., 0.7 g., 0.7 g., and 1.2 g.). The serum calcium was

8.6 mg./100 ml., inorganic phosphate 3.6 mg./100 ml., and alkaline

phosphatase 8.3 King-Armstrong units/100 ml.

She became progressively more drowsy and had infrequent generalized

convulsions. Biopsy of an epitrochlear node and an area of

skin infiltration was performed on 25 January. Since her general

condition was deteriorating rapidly and sarcoidosis was the only

treatable condition compatible with the signs, she was given prednisone

40 mg. daily while the result of the biopsy was awaited. There

was a dramatic improvement in her mental and physical condition

within 48 hours. The histological features of both gland and skin

infiltration were those of sarcoidosis. The prednisone was reduced

over four weeks to a maintenance dose of 10 mg. daily, which was

further reduced to 5 mg. in May 1963.

When she was readmitted in May 1963 for reassessment the skin

infiltrations were contracted, wrinkled, and depressed, and were a

greyish purple colour. No lymph nodes were palpable. The subcutaneous

nodule on the abdominal wall had disappeared and the

nodule on the left forearm was much smaller. The swelling of the

fingers had subsided and a radiograph showed that recalcification

of the phalanges had begun. The only neurological abnormality

was that the plantar responses were extensor.

The cerebrospinal fluid was now normal: there was 1 lymphocyte/

c.mm., protein 40 mg./100 ml., sugar 49 mg./100 ml., and chloride

710 mEq/l. The erythrocyte sedimentation rate was 35 mm.

In August 1963 the E.S.R. had fallen to 30 mm. in one hour.

The total serum protein was 6.5 g./100 ml., of which 3.35 g. was

albumin and 3.15 g. globulin; the electrophoretic pattern was

normal.

COMMENT

The response to treatment with adrenal corticosteroids in

patients with sarcoidosis of the central nervous system is unpredictable

and is often disappointing. The signs and

symptoms may diminish spontaneously without treatment.

This patient was critically ill before treatment, the clinical

response was dramatic, and the cerebrospinal fluid returned to

normal. A similar response to treatment with adrenal corticosteroids

was obtained in the only other case of acute sarcoid

meningo-encephaliti s that is recorded as having been treated

in this way (Carstensen and Norviit 1953).

Neurological signs may develop when there is no evidence of

sarcoid elsewhere, though six of seven patients described by

(1961) had at one time had demonstrable pulmonary

involvement, which in one case was apparent only in a chest

radiograph taken 10 years earlier.

Sarcoidosis should always be considered in the differential

diagnosis of a patient with meningo-encephaliti s, because the

response to treatment with adrenal corticosteroids is excellent.

I am grateful to Dr. W. D. Brinton for permission to report his

case.

PETER RICHARDS, M.A., M.B., M.R.C.P.

-St. 's Hospital, London.

REFERENCES

Carstensen, B., and Norviit, L. (1953). Nord. Med., 49, 299.

, A. G. (1961). Postgrad. med. Y., 37, 431.

From: D. <dmatt1960 (AT) yahoo (DOT) com>To: neurosarcoidosis@ yahoogroups. comSent: Tue, January 19, 2010 6:24:07 PMSubject: Off Line

Finally getting back into reading posts. I apologize for being remiss on birthdays and saying hello. Been a rough patch here with , After a weekend trip to my brothers she came home weak & disoriented. At first I thought it was just being over tired, but now it seems to be more than that. Lately trips away from home are taking a tremendous toll on her. I am finding that her speech patterns are really bad and so is her mobility. Doctors say it is to be expected, but I keep asking why if the meds are supposedly working? Sorry I am venting, but does anyone have any suggestions regard to this. Thanks matt

[Guest guest]



Give 'em hell.

Off Line

Finally getting back into reading posts. I apologize for being remiss on birthdays and saying hello. Been a rough patch here with , After a weekend trip to my brothers she came home weak & disoriented. At first I thought it was just being over tired, but now it seems to be more than that. Lately trips away from home are taking a tremendous toll on her. I am finding that her speech patterns are really bad and so is her mobility. Doctors say it is to be expected, but I keep asking why if the meds are supposedly working? Sorry I am venting, but does anyone have any suggestions regard to this. Thanks matt

[Guest guest]

Thanks. I keep trying.Matt

From: tracie feldhaus <tiodaat2001@ yahoo.com>Subject: Re: Matt--meningitis- encephalitisTo: Neurosarcoidosis@ yahoogroups. comDate: Wednesday, January 20, 2010, 10:36 AM

Matt,

It sounds like she's gotten alot worse with the Cellcept? Sounds like this drug is not her magic bullet. Her M.D.'s "this is to be expected" is bull. She shouldn't be getting worse if the meds the right one. Rarely does sarc progress this quickly- have they done a spinal tap to make sure she doesn't have some meningitis-encephal itis going on?

Darlene is right you need second opinions on this-- they are missing something.

Here is an article that was written in 1964--

1576 19 DecAber 1964

Medical Memoranda

Acute Sarcoid Meningo-encephaliti s

Brit. mAd. _., 1964, 2, 1576

Meningo-encephaliti s is a rare complication of sarcoidosis. The

onset may be abrupt and deterioration rapid. Failure to be

aware of this may result in the death of a patient with a treatable

condition.

CASE REPORT

A woman aged 42 was admitted to hospital on 22 January 1963

having had several generalized convulsions early that morning.

There was no family history of epilepsy. The only information

available on admission was that

her weight had fallen by 35 kg.

in two years and that she had

been drowsy the previous day.

She was drowsy, disorientated,

and incontinent of

_| | 9- urine and faeces. Though her

neck was stiff, Kernig's sign

was not present. Both plantar

responses were extensor.

Examination of sensory nerve

function was unreliable on

account of lack of co-operation,

but subsequent examinations

did not reveal any

sensory loss.- The optic fundi

were normal and there were no

cranial nerve lesions.-

There were numerous purple

areas of skin infiltration

which were raised, irregular in

outline, and varied from 1 to

6 cm. in greatest diameter.

They were confined to the face,

back of the chest, and arms,

particularly the upper arms;

the lesions tended to be symmetrical.

There were two

subcutaneous nodules without

associated skin infiltration, one

on the left forearm and the

other on the anterior abdominal

wall.

Large, rubbery, and discrete

lymph nodes were palpable in

the neck, supraclavicular

fossae., axillae, epitrochlear

Cystic and destructive changes in the regions, and groins. The left

phalanges, January 1963. little finger and the right

middle finger were swollen.

The liver and spleen were not palpable. Her temperature was

normal. The chest radiograph was normal, but films of the

hands revealed destructive changes (see Fig.).

The lumbar cerebrospinal fluid contained 8 lymphocytes/ c.mm.,

protein 250 mg./100 ml., sugar 18 mg./100 ml., and chloride 730

mEq/l. The Wassermann reaction was negative. The results of

other investigations were haemoglobin 14.7 g./100 ml., erythrocyte

sedimentabtin rate 32 mm. in one hour (Wintrobe), and total serum

proteins 5.2 g./100 ml., of which 2.4 g. was albumin and 2.8 g.

globulin (0.3 g., 0.7 g., 0.7 g., and 1.2 g.). The serum calcium was

8.6 mg./100 ml., inorganic phosphate 3.6 mg./100 ml., and alkaline

phosphatase 8.3 King-Armstrong units/100 ml.

She became progressively more drowsy and had infrequent generalized

convulsions. Biopsy of an epitrochlear node and an area of

skin infiltration was performed on 25 January. Since her general

condition was deteriorating rapidly and sarcoidosis was the only

treatable condition compatible with the signs, she was given prednisone

40 mg. daily while the result of the biopsy was awaited. There

was a dramatic improvement in her mental and physical condition

within 48 hours. The histological features of both gland and skin

infiltration were those of sarcoidosis. The prednisone was reduced

over four weeks to a maintenance dose of 10 mg. daily, which was

further reduced to 5 mg. in May 1963.

When she was readmitted in May 1963 for reassessment the skin

infiltrations were contracted, wrinkled, and depressed, and were a

greyish purple colour. No lymph nodes were palpable. The subcutaneous

nodule on the abdominal wall had disappeared and the

nodule on the left forearm was much smaller. The swelling of the

fingers had subsided and a radiograph showed that recalcification

of the phalanges had begun. The only neurological abnormality

was that the plantar responses were extensor.

The cerebrospinal fluid was now normal: there was 1 lymphocyte/

c.mm., protein 40 mg./100 ml., sugar 49 mg./100 ml., and chloride

710 mEq/l. The erythrocyte sedimentation rate was 35 mm.

In August 1963 the E.S.R. had fallen to 30 mm. in one hour.

The total serum protein was 6.5 g./100 ml., of which 3.35 g. was

albumin and 3.15 g. globulin; the electrophoretic pattern was

normal.

COMMENT

The response to treatment with adrenal corticosteroids in

patients with sarcoidosis of the central nervous system is unpredictable

and is often disappointing. The signs and

symptoms may diminish spontaneously without treatment.

This patient was critically ill before treatment, the clinical

response was dramatic, and the cerebrospinal fluid returned to

normal. A similar response to treatment with adrenal corticosteroids

was obtained in the only other case of acute sarcoid

meningo-encephaliti s that is recorded as having been treated

in this way (Carstensen and Norviit 1953).

Neurological signs may develop when there is no evidence of

sarcoid elsewhere, though six of seven patients described by

(1961) had at one time had demonstrable pulmonary

involvement, which in one case was apparent only in a chest

radiograph taken 10 years earlier.

Sarcoidosis should always be considered in the differential

diagnosis of a patient with meningo-encephaliti s, because the

response to treatment with adrenal corticosteroids is excellent.

I am grateful to Dr. W. D. Brinton for permission to report his

case.

PETER RICHARDS, M.A., M.B., M.R.C.P.

-St. 's Hospital, London.

REFERENCES

Carstensen, B., and Norviit, L. (1953). Nord. Med., 49, 299.

, A. G. (1961). Postgrad. med. Y., 37, 431.

From: D. <dmatt1960 (AT) yahoo (DOT) com>To: neurosarcoidosis@ yahoogroups. comSent: Tue, January 19, 2010 6:24:07 PMSubject: Off Line

Finally getting back into reading posts. I apologize for being remiss on birthdays and saying hello. Been a rough patch here with , After a weekend trip to my brothers she came home weak & disoriented. At first I thought it was just being over tired, but now it seems to be more than that. Lately trips away from home are taking a tremendous toll on her. I am finding that her speech patterns are really bad and so is her mobility. Doctors say it is to be expected, but I keep asking why if the meds are supposedly working? Sorry I am venting, but does anyone have any suggestions regard to this. Thanks matt

[Guest guest]

Thanks. We are getting back to as "normal" as we can. I guess my question now is why does this happen? You attempt to go away for a few days & visit family etc and it takes such a horrible toll on her. MattFrom: tracie feldhaus <tiodaat2001@

yahoo.com>Subject: Re: Matt--meningitis- encephalitisTo: Neurosarcoidosis@ yahoogroups. comDate: Wednesday, January 20, 2010, 10:36 AM

Matt,

It sounds like she's gotten alot worse with the Cellcept? Sounds like this drug is not her magic bullet. Her M.D.'s "this is to be expected" is bull. She shouldn't be getting worse if the meds the right one. Rarely does sarc progress this quickly- have they done a spinal tap to make sure she doesn't have some meningitis-encephal itis going on?

Darlene is right you need second opinions on this-- they are missing something.

Here is an article that was written in 1964--

1576 19 DecAber 1964

Medical Memoranda

Acute Sarcoid Meningo-encephaliti s

Brit. mAd. _., 1964, 2, 1576

Meningo-encephaliti s is a rare complication of sarcoidosis. The

onset may be abrupt and deterioration rapid. Failure to be

aware of this may result in the death of a patient with a treatable

condition.

CASE REPORT

A woman aged 42 was admitted to hospital on 22 January 1963

having had several generalized convulsions early that morning.

There was no family history of epilepsy. The only information

available on admission was that

her weight had fallen by 35 kg.

in two years and that she had

been drowsy the previous day.

She was drowsy, disorientated,

and incontinent of

_| | 9- urine and faeces. Though her

neck was stiff, Kernig's sign

was not present. Both plantar

responses were extensor.

Examination of sensory nerve

function was unreliable on

account of lack of co-operation,

but subsequent examinations

did not reveal any

sensory loss.- The optic fundi

were normal and there were no

cranial nerve lesions.-

There were numerous purple

areas of skin infiltration

which were raised, irregular in

outline, and varied from 1 to

6 cm. in greatest diameter.

They were confined to the face,

back of the chest, and arms,

particularly the upper arms;

the lesions tended to be symmetrical.

There were two

subcutaneous nodules without

associated skin infiltration, one

on the left forearm and the

other on the anterior abdominal

wall.

Large, rubbery, and discrete

lymph nodes were palpable in

the neck, supraclavicular

fossae., axillae, epitrochlear

Cystic and destructive changes in the regions, and groins. The left

phalanges, January 1963. little finger and the right

middle finger were swollen.

The liver and spleen were not palpable. Her temperature was

normal. The chest radiograph was normal, but films of the

hands revealed destructive changes (see Fig.).

The lumbar cerebrospinal fluid contained 8 lymphocytes/ c.mm.,

protein 250 mg./100 ml., sugar 18 mg./100 ml., and chloride 730

mEq/l. The Wassermann reaction was negative. The results of

other investigations were haemoglobin 14.7 g./100 ml., erythrocyte

sedimentabtin rate 32 mm. in one hour (Wintrobe), and total serum

proteins 5.2 g./100 ml., of which 2.4 g. was albumin and 2.8 g.

globulin (0.3 g., 0.7 g., 0.7 g., and 1.2 g.). The serum calcium was

8.6 mg./100 ml., inorganic phosphate 3.6 mg./100 ml., and alkaline

phosphatase 8.3 King-Armstrong units/100 ml.

She became progressively more drowsy and had infrequent generalized

convulsions. Biopsy of an epitrochlear node and an area of

skin infiltration was performed on 25 January. Since her general

condition was deteriorating rapidly and sarcoidosis was the only

treatable condition compatible with the signs, she was given prednisone

40 mg. daily while the result of the biopsy was awaited. There

was a dramatic improvement in her mental and physical condition

within 48 hours. The histological features of both gland and skin

infiltration were those of sarcoidosis. The prednisone was reduced

over four weeks to a maintenance dose of 10 mg. daily, which was

further reduced to 5 mg. in May 1963.

When she was readmitted in May 1963 for reassessment the skin

infiltrations were contracted, wrinkled, and depressed, and were a

greyish purple colour. No lymph nodes were palpable. The subcutaneous

nodule on the abdominal wall had disappeared and the

nodule on the left forearm was much smaller. The swelling of the

fingers had subsided and a radiograph showed that recalcification

of the phalanges had begun. The only neurological abnormality

was that the plantar responses were extensor.

The cerebrospinal fluid was now normal: there was 1 lymphocyte/

c.mm., protein 40 mg./100 ml., sugar 49 mg./100 ml., and chloride

710 mEq/l. The erythrocyte sedimentation rate was 35 mm.

In August 1963 the E.S.R. had fallen to 30 mm. in one hour.

The total serum protein was 6.5 g./100 ml., of which 3.35 g. was

albumin and 3.15 g. globulin; the electrophoretic pattern was

normal.

COMMENT

The response to treatment with adrenal corticosteroids in

patients with sarcoidosis of the central nervous system is unpredictable

and is often disappointing. The signs and

symptoms may diminish spontaneously without treatment.

This patient was critically ill before treatment, the clinical

response was dramatic, and the cerebrospinal fluid returned to

normal. A similar response to treatment with adrenal corticosteroids

was obtained in the only other case of acute sarcoid

meningo-encephaliti s that is recorded as having been treated

in this way (Carstensen and Norviit 1953).

Neurological signs may develop when there is no evidence of

sarcoid elsewhere, though six of seven patients described by

(1961) had at one time had demonstrable pulmonary

involvement, which in one case was apparent only in a chest

radiograph taken 10 years earlier.

Sarcoidosis should always be considered in the differential

diagnosis of a patient with meningo-encephaliti s, because the

response to treatment with adrenal corticosteroids is excellent.

I am grateful to Dr. W. D. Brinton for permission to report his

case.

PETER RICHARDS, M.A., M.B., M.R.C.P.

-St. 's Hospital, London.

REFERENCES

Carstensen, B., and Norviit, L. (1953). Nord. Med., 49, 299.

, A. G. (1961). Postgrad. med. Y., 37, 431.

From: D. <dmatt1960 (AT) yahoo (DOT) com>To: neurosarcoidosis@ yahoogroups. comSent: Tue, January 19, 2010 6:24:07 PMSubject: Off Line

Finally getting back into reading posts. I apologize for being remiss on birthdays and saying hello. Been a rough patch here with , After a weekend trip to my brothers she came home weak & disoriented. At first I thought it was just being over tired, but now it seems to be more than that. Lately trips away from home are taking a tremendous toll on her. I am finding that her speech patterns are really bad and so is her mobility. Doctors say it is to be expected, but I keep asking why if the meds are supposedly working? Sorry I am venting, but does anyone have any suggestions regard to this. Thanks matt