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In 2008, age 76 years, I developed left sided lancinating facial pains, perhaps three quarters to one second apart and in three- to four-second epochs, followed by a pause of a few seconds until the next paroxysm. Any speech, oral stimulation or merely a change in facial expression was sufficient to trigger pain—I dared not grimace.

After a few days in one of the severer periods of consuming paracetamol and tramadol, I became desperate with 90 minutes of almost continuous spasms. My daughter, with whom I live, called an ambulance. En route to hospital I inhaled deeply the nitrous oxide/oxygen blend, in the manner of a woman in established labour. As we arrived at the emergency room, the pain ceased and I decided to return home, given a lengthy wait for medical attention.

For the next decade I suffered to a greater or lesser extent with trigeminal neuralgia (TN). I was never completely free of the affliction, at best occasional bouts, at worst, periods of two or three weeks when I needed to lie down and use strong analgesics. I could not touch or wash my left face, swim, blow my nose or pull shirts on over my head. To shave, wash my hair or clean my teeth needed great care. Pain was most prevalent in the first hour or two of the morning, particularly when straining to pass stool. One of the attacks ‘to live in infamy’ occurred with a piece of chocolate in my mouth, with severe split-second flashes of neuralgia at three per second. I had to rush to the bathroom to rinse my mouth for immediate relief. It seemed sweet taste was involved although I thought taste went via the seventh cranial nerve—perhaps not always.

I saw a neurologist, but his drug treatments were poorly effective. Carbamazepine did not provide the anticipated relief and I felt agitated on this but gave it a good trial. Gabapentin up to 600mg four times daily, as much as I could tolerate, reduced the severity of bouts modestly but not the frequency. Baclofen 60mg a day did not help. Amitriptyline 20mg caused an anxiety state after three weeks. Clonazepam 0.5mg knocked me out for six hours, but the drug-induced rest was helpful in acute situations. I did my own research and was soon watching a microvascular decompression on YouTube. I saw a neurosurgeon, but he was reluctant to operate; I was too old.

The pain was brutal and, during severe bouts, I was best to lie supine, relax and try to stay calm. I seldom had the TN pain during sleeping hours (provided I kept off my left side). The cardiologist in me correlated this lack of TN pain with a lower nocturnal blood pressure (BP) and again the highest BPs in the first hours after rising as documented on my 24hr BP record, with the worst period of pain. I was taking treatment for mild hypertension (Felodipine 5mg and a diuretic) but considered whether more rigorous BP control might be useful. I decided to escalate treatment, achieving a mean systolic pressure of 70mmHg at night and 90–100mmHg in the day by adding candesartan, eventually at a high dose of 32mg. I was surprised that I could tolerate a systolic pressure in the 90s while up and at work with so little symptomatic hypotension but kept a careful watch on my BP with this approach to self-management. My pain was then much better controlled—not perfect, but for several years I was much more comfortable, could work and I had not enjoyed such sustained relief until my BP was this low.

I am now 88 years old. Four years ago, the TN returned despite my low BP. The usual trigger point for the pain was either lateral to the left upper lip, less commonly in the scalp, near the hairline. A second neurologist was consulted. Mexiletine produced ataxia; prednisone was unhelpful; oxcarbazepine had a slight benefit but made me groggy. A repeat MRI showed a vascular impingement of the fifth nerve root but did not change a different surgeon’s recommendation—still too old.

Then it happened, the accidental cure of my TN. Two years ago, I lay down after an evening meal on my bed watching TV and went to sleep. I woke at 11pm with some numbness right leg and when I stood up, the limb was limp. I fell, striking my forehead with extreme force on a wooden stool, about 20cm off the floor, without loss of consciousness. Thinking I may have had a stroke but then realizing it was a flaccid weakness—it will recover. But I realized I was bleeding from the scalp, where my TN trigger point was located at the time (Figure 1). My daughter, who knew I could not tolerate any sensory stimulus to this area, was reluctant to stem the bleeding but this was essential and to my surprise did not cause pain. In hospital, seven stitches were necessary.

Figure 1: The result of the fall.

For two years I have had no TN pain, other than after vigorously blowing my nose with a slight hint of “be careful” warning. I was able to reduce my BP treatment. I could now tolerate all stimuli to my face, even swim and wash, and perform my ablutions without fear of the ‘tic doloreaux’.

My understanding of TN is that it is usually related to a vascular compression of the trigeminal nerve root near the brainstem by a stiff and tortuous artery. Arterial pulsations gradually lead to demyelination of the sensory fibres in the nerve root, leading to short circuiting of electrical impulses from these fibres to neighbouring unmyelinated pain nerve fibres. Thus a touch or stretch sensory receptor starting an electrical signal to indicate touch or stretch arrives at the brain in a group of pain fibres and the subject feels pain, not touch or stretch.

Hypertension is a predisposing factor for arterial tortuosity and treatment may have reduced the pressure on my trigeminal root. Epidemiological data provides some support for HT as a risk factor for TN,1 but its reduction doesn’t seem to have been trialed as a possible treatment. I would suggest that the possibility of treatment by BP reduction could do with further study. It seemed to work in me.

What might have happened with the blow to the head? My head was in free fall for 1.5 metres and was brought to a stop in 0.005 metres (the depth of my skin laceration and small bone give) so the negative G force on the contents of my head would be very high. (by using the formula V2=U2+2as on the above figures gives a decelerating force of around 300G!). The resulting shock waves in head contents (compression and stretching) and Newton’s first law on the more dense artery and also the brain stem would reset the nerve/artery relationship, the kinked artery being far less fixed than the nerve root. The artery was moved sufficiently away from the nerve root and stayed away.

Although such drastic treatment of the head is not available for treatment, there may be less dramatic ways of applying G forces to the head or pressure waves in the CSF that could be considered as the basis for a possible curative treatment. But whatever the mechanism, the fall and sudden deceleration injury does seem to have cured my neuralgia.

Alas, as if this were not enough for one physician, I have developed motor neuron disease—hence the third neurologist, who encouraged me to contribute these observations.

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Denis Friedlander, Retired Cardiologist, Hamilton.

Acknowledgements

Dr A Chancellor suggested this piece and edited an earlier draft.

Correspondence

Denis Friedlander, Retired Cardiologist, Hamilton.

Correspondence Email

denisf@xtra.co.nz

Competing Interests

Nil.

1. Pan SL, Yen MF, Chiu YH, et al. Increased risk of trigeminal neuralgia after hypertension: A population-based study. Neurology. 2011; 77(17):1605–1610.

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

In 2008, age 76 years, I developed left sided lancinating facial pains, perhaps three quarters to one second apart and in three- to four-second epochs, followed by a pause of a few seconds until the next paroxysm. Any speech, oral stimulation or merely a change in facial expression was sufficient to trigger pain—I dared not grimace.

After a few days in one of the severer periods of consuming paracetamol and tramadol, I became desperate with 90 minutes of almost continuous spasms. My daughter, with whom I live, called an ambulance. En route to hospital I inhaled deeply the nitrous oxide/oxygen blend, in the manner of a woman in established labour. As we arrived at the emergency room, the pain ceased and I decided to return home, given a lengthy wait for medical attention.

For the next decade I suffered to a greater or lesser extent with trigeminal neuralgia (TN). I was never completely free of the affliction, at best occasional bouts, at worst, periods of two or three weeks when I needed to lie down and use strong analgesics. I could not touch or wash my left face, swim, blow my nose or pull shirts on over my head. To shave, wash my hair or clean my teeth needed great care. Pain was most prevalent in the first hour or two of the morning, particularly when straining to pass stool. One of the attacks ‘to live in infamy’ occurred with a piece of chocolate in my mouth, with severe split-second flashes of neuralgia at three per second. I had to rush to the bathroom to rinse my mouth for immediate relief. It seemed sweet taste was involved although I thought taste went via the seventh cranial nerve—perhaps not always.

I saw a neurologist, but his drug treatments were poorly effective. Carbamazepine did not provide the anticipated relief and I felt agitated on this but gave it a good trial. Gabapentin up to 600mg four times daily, as much as I could tolerate, reduced the severity of bouts modestly but not the frequency. Baclofen 60mg a day did not help. Amitriptyline 20mg caused an anxiety state after three weeks. Clonazepam 0.5mg knocked me out for six hours, but the drug-induced rest was helpful in acute situations. I did my own research and was soon watching a microvascular decompression on YouTube. I saw a neurosurgeon, but he was reluctant to operate; I was too old.

The pain was brutal and, during severe bouts, I was best to lie supine, relax and try to stay calm. I seldom had the TN pain during sleeping hours (provided I kept off my left side). The cardiologist in me correlated this lack of TN pain with a lower nocturnal blood pressure (BP) and again the highest BPs in the first hours after rising as documented on my 24hr BP record, with the worst period of pain. I was taking treatment for mild hypertension (Felodipine 5mg and a diuretic) but considered whether more rigorous BP control might be useful. I decided to escalate treatment, achieving a mean systolic pressure of 70mmHg at night and 90–100mmHg in the day by adding candesartan, eventually at a high dose of 32mg. I was surprised that I could tolerate a systolic pressure in the 90s while up and at work with so little symptomatic hypotension but kept a careful watch on my BP with this approach to self-management. My pain was then much better controlled—not perfect, but for several years I was much more comfortable, could work and I had not enjoyed such sustained relief until my BP was this low.

I am now 88 years old. Four years ago, the TN returned despite my low BP. The usual trigger point for the pain was either lateral to the left upper lip, less commonly in the scalp, near the hairline. A second neurologist was consulted. Mexiletine produced ataxia; prednisone was unhelpful; oxcarbazepine had a slight benefit but made me groggy. A repeat MRI showed a vascular impingement of the fifth nerve root but did not change a different surgeon’s recommendation—still too old.

Then it happened, the accidental cure of my TN. Two years ago, I lay down after an evening meal on my bed watching TV and went to sleep. I woke at 11pm with some numbness right leg and when I stood up, the limb was limp. I fell, striking my forehead with extreme force on a wooden stool, about 20cm off the floor, without loss of consciousness. Thinking I may have had a stroke but then realizing it was a flaccid weakness—it will recover. But I realized I was bleeding from the scalp, where my TN trigger point was located at the time (Figure 1). My daughter, who knew I could not tolerate any sensory stimulus to this area, was reluctant to stem the bleeding but this was essential and to my surprise did not cause pain. In hospital, seven stitches were necessary.

Figure 1: The result of the fall.

For two years I have had no TN pain, other than after vigorously blowing my nose with a slight hint of “be careful” warning. I was able to reduce my BP treatment. I could now tolerate all stimuli to my face, even swim and wash, and perform my ablutions without fear of the ‘tic doloreaux’.

My understanding of TN is that it is usually related to a vascular compression of the trigeminal nerve root near the brainstem by a stiff and tortuous artery. Arterial pulsations gradually lead to demyelination of the sensory fibres in the nerve root, leading to short circuiting of electrical impulses from these fibres to neighbouring unmyelinated pain nerve fibres. Thus a touch or stretch sensory receptor starting an electrical signal to indicate touch or stretch arrives at the brain in a group of pain fibres and the subject feels pain, not touch or stretch.

Hypertension is a predisposing factor for arterial tortuosity and treatment may have reduced the pressure on my trigeminal root. Epidemiological data provides some support for HT as a risk factor for TN,1 but its reduction doesn’t seem to have been trialed as a possible treatment. I would suggest that the possibility of treatment by BP reduction could do with further study. It seemed to work in me.

What might have happened with the blow to the head? My head was in free fall for 1.5 metres and was brought to a stop in 0.005 metres (the depth of my skin laceration and small bone give) so the negative G force on the contents of my head would be very high. (by using the formula V2=U2+2as on the above figures gives a decelerating force of around 300G!). The resulting shock waves in head contents (compression and stretching) and Newton’s first law on the more dense artery and also the brain stem would reset the nerve/artery relationship, the kinked artery being far less fixed than the nerve root. The artery was moved sufficiently away from the nerve root and stayed away.

Although such drastic treatment of the head is not available for treatment, there may be less dramatic ways of applying G forces to the head or pressure waves in the CSF that could be considered as the basis for a possible curative treatment. But whatever the mechanism, the fall and sudden deceleration injury does seem to have cured my neuralgia.

Alas, as if this were not enough for one physician, I have developed motor neuron disease—hence the third neurologist, who encouraged me to contribute these observations.

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Denis Friedlander, Retired Cardiologist, Hamilton.

Acknowledgements

Dr A Chancellor suggested this piece and edited an earlier draft.

Correspondence

Denis Friedlander, Retired Cardiologist, Hamilton.

Correspondence Email

denisf@xtra.co.nz

Competing Interests

Nil.

1. Pan SL, Yen MF, Chiu YH, et al. Increased risk of trigeminal neuralgia after hypertension: A population-based study. Neurology. 2011; 77(17):1605–1610.

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

In 2008, age 76 years, I developed left sided lancinating facial pains, perhaps three quarters to one second apart and in three- to four-second epochs, followed by a pause of a few seconds until the next paroxysm. Any speech, oral stimulation or merely a change in facial expression was sufficient to trigger pain—I dared not grimace.

After a few days in one of the severer periods of consuming paracetamol and tramadol, I became desperate with 90 minutes of almost continuous spasms. My daughter, with whom I live, called an ambulance. En route to hospital I inhaled deeply the nitrous oxide/oxygen blend, in the manner of a woman in established labour. As we arrived at the emergency room, the pain ceased and I decided to return home, given a lengthy wait for medical attention.

For the next decade I suffered to a greater or lesser extent with trigeminal neuralgia (TN). I was never completely free of the affliction, at best occasional bouts, at worst, periods of two or three weeks when I needed to lie down and use strong analgesics. I could not touch or wash my left face, swim, blow my nose or pull shirts on over my head. To shave, wash my hair or clean my teeth needed great care. Pain was most prevalent in the first hour or two of the morning, particularly when straining to pass stool. One of the attacks ‘to live in infamy’ occurred with a piece of chocolate in my mouth, with severe split-second flashes of neuralgia at three per second. I had to rush to the bathroom to rinse my mouth for immediate relief. It seemed sweet taste was involved although I thought taste went via the seventh cranial nerve—perhaps not always.

I saw a neurologist, but his drug treatments were poorly effective. Carbamazepine did not provide the anticipated relief and I felt agitated on this but gave it a good trial. Gabapentin up to 600mg four times daily, as much as I could tolerate, reduced the severity of bouts modestly but not the frequency. Baclofen 60mg a day did not help. Amitriptyline 20mg caused an anxiety state after three weeks. Clonazepam 0.5mg knocked me out for six hours, but the drug-induced rest was helpful in acute situations. I did my own research and was soon watching a microvascular decompression on YouTube. I saw a neurosurgeon, but he was reluctant to operate; I was too old.

The pain was brutal and, during severe bouts, I was best to lie supine, relax and try to stay calm. I seldom had the TN pain during sleeping hours (provided I kept off my left side). The cardiologist in me correlated this lack of TN pain with a lower nocturnal blood pressure (BP) and again the highest BPs in the first hours after rising as documented on my 24hr BP record, with the worst period of pain. I was taking treatment for mild hypertension (Felodipine 5mg and a diuretic) but considered whether more rigorous BP control might be useful. I decided to escalate treatment, achieving a mean systolic pressure of 70mmHg at night and 90–100mmHg in the day by adding candesartan, eventually at a high dose of 32mg. I was surprised that I could tolerate a systolic pressure in the 90s while up and at work with so little symptomatic hypotension but kept a careful watch on my BP with this approach to self-management. My pain was then much better controlled—not perfect, but for several years I was much more comfortable, could work and I had not enjoyed such sustained relief until my BP was this low.

I am now 88 years old. Four years ago, the TN returned despite my low BP. The usual trigger point for the pain was either lateral to the left upper lip, less commonly in the scalp, near the hairline. A second neurologist was consulted. Mexiletine produced ataxia; prednisone was unhelpful; oxcarbazepine had a slight benefit but made me groggy. A repeat MRI showed a vascular impingement of the fifth nerve root but did not change a different surgeon’s recommendation—still too old.

Then it happened, the accidental cure of my TN. Two years ago, I lay down after an evening meal on my bed watching TV and went to sleep. I woke at 11pm with some numbness right leg and when I stood up, the limb was limp. I fell, striking my forehead with extreme force on a wooden stool, about 20cm off the floor, without loss of consciousness. Thinking I may have had a stroke but then realizing it was a flaccid weakness—it will recover. But I realized I was bleeding from the scalp, where my TN trigger point was located at the time (Figure 1). My daughter, who knew I could not tolerate any sensory stimulus to this area, was reluctant to stem the bleeding but this was essential and to my surprise did not cause pain. In hospital, seven stitches were necessary.

Figure 1: The result of the fall.

For two years I have had no TN pain, other than after vigorously blowing my nose with a slight hint of “be careful” warning. I was able to reduce my BP treatment. I could now tolerate all stimuli to my face, even swim and wash, and perform my ablutions without fear of the ‘tic doloreaux’.

My understanding of TN is that it is usually related to a vascular compression of the trigeminal nerve root near the brainstem by a stiff and tortuous artery. Arterial pulsations gradually lead to demyelination of the sensory fibres in the nerve root, leading to short circuiting of electrical impulses from these fibres to neighbouring unmyelinated pain nerve fibres. Thus a touch or stretch sensory receptor starting an electrical signal to indicate touch or stretch arrives at the brain in a group of pain fibres and the subject feels pain, not touch or stretch.

Hypertension is a predisposing factor for arterial tortuosity and treatment may have reduced the pressure on my trigeminal root. Epidemiological data provides some support for HT as a risk factor for TN,1 but its reduction doesn’t seem to have been trialed as a possible treatment. I would suggest that the possibility of treatment by BP reduction could do with further study. It seemed to work in me.

What might have happened with the blow to the head? My head was in free fall for 1.5 metres and was brought to a stop in 0.005 metres (the depth of my skin laceration and small bone give) so the negative G force on the contents of my head would be very high. (by using the formula V2=U2+2as on the above figures gives a decelerating force of around 300G!). The resulting shock waves in head contents (compression and stretching) and Newton’s first law on the more dense artery and also the brain stem would reset the nerve/artery relationship, the kinked artery being far less fixed than the nerve root. The artery was moved sufficiently away from the nerve root and stayed away.

Although such drastic treatment of the head is not available for treatment, there may be less dramatic ways of applying G forces to the head or pressure waves in the CSF that could be considered as the basis for a possible curative treatment. But whatever the mechanism, the fall and sudden deceleration injury does seem to have cured my neuralgia.

Alas, as if this were not enough for one physician, I have developed motor neuron disease—hence the third neurologist, who encouraged me to contribute these observations.

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Denis Friedlander, Retired Cardiologist, Hamilton.

Acknowledgements

Dr A Chancellor suggested this piece and edited an earlier draft.

Correspondence

Denis Friedlander, Retired Cardiologist, Hamilton.

Correspondence Email

denisf@xtra.co.nz

Competing Interests

Nil.

1. Pan SL, Yen MF, Chiu YH, et al. Increased risk of trigeminal neuralgia after hypertension: A population-based study. Neurology. 2011; 77(17):1605–1610.

Contact diana@nzma.org.nz
for the PDF of this article

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