Monday 18 May 2015

Cesation of a seizure disorder - correction of The Atlas Subluxation Complex

CESSATION OF A SEIZURE DISORDER: Correction of the Atlas Subluxation Complex

Robert J. Goodman, D.C., John S. Mosby Jr., D.C., M.D.

ABSTRACT

Observations of one patient presenting with a seizure disorder are reported. Relief of symptoms is

noted subsequent to correction of the misalignment of the occipito-atlanto-axial complex. The authors

suggest a relationship between the misaligned skull and subjacent vertebrae and some seizure disorders.

Key Words: epilepsy; atlanto-occipital joint

INTRODUCTION

The term epilepsy refers to any disorder characterized by recurrent seizures. Seizures are transient

disturbances of cerebral function due to abnormal paroxysmal neuronal discharges in the brain.

Approximately 0.5% of the U.S. population is affected. 1, 2



Epilepsy is grouped into two different etiological categories, idiopathic or constitutional and

symptomatic epilepsy. In idiopathic or constitutional epilepsy, seizures usually begin between 5 and 20

years of age. NO specific cause can be identified, and there are no other neurological abnormalities.1 The



causes of symptomatic epilepsy include abnormalities and perinatal injuries, disorders of metabolism,

trauma, space-occupying lesions, vascular problems, degenerative disorders, and infectious diseases. 1, 3-6



Clinically, seizures are categorized by description. The two major descriptive classifications are

partial seizures and generalized seizures. Partial seizures are determined by clinical observation and by

electroencephalograph manifestations. They affect only a restricted part of one cerebral hemisphere. In

simple partial seizures the patient remains conscious, but in complex partial seizures consciousness is lost.

Partial seizures may evolve into generalized seizures.1



Generalized seizures are categorized as petit mal or absence seizures, atypical seizures, myclonic

seizures, akinetic seizures, grand mal or tonic-clonic seizures, atonic or ionic seizures, and seizures that will

not fit into any other category.

Absence or petit mal seizures cause some reduction in postural tone, with some clonic or tonic

components. Consciousness is impaired. These attacks occur quickly. When the attack occurs as a person

is speaking, the person may miss a few words in mid-sentence then resume with the remainder of the

sentence when the attack subsides. If a child has a petit mal seizure while playing, for instance, he or she

may freeze, that is, stand perfectly still while reaching for a toy. These seizures will often cease at

approximately 20 years of age. Diagnosis is assisted by electroencephalographic studies which show

bilateral synchronous and symmetric 3Hz spike-and-wave activity.1



Atypical seizures are almost identical to the petit mal seizure except that changes in tone are more

dramatic and onset and termination of the attack is slower.1



Myclonic seizures cause single or multiple myclonic jerks and myofacial spikes are seen on an

EEG.1 Akinetic seizures present as a sudden loss of consciousness and EEG findings show synchronous

firing from deep lesions often in the frontal regions of the brain.7



The grand-mal or tonic-clonic seizure occurs with a sudden loss of consciousness, the patient

becomes rigid then falls to the ground and respiration is arrested for less than 60 seconds. This is described

as the tonic phase. The next phase is the clonic phase during which the body jerks violently for 2 to 3

minutes. Flaccid coma occurs next. During this type of seizure the tongue may be bitten and urinary or

fecal continence may be lost. The patient will then either recover consciousness, drift into sleep, or never

recover consciousness which is called status epilepticus.1



Atonic seizures are epileptic drop attacks where the patient, usually a child, loses all motor tone

and falls to the ground.8 The stigma of the helmet is often conferred of necessity on the patient with drop



attacks in order to protect him from further injury during these ictal events. These spells are often

intractable to treatment. Finally, the onset of ictal falling almost always occurs in patients who already

have one of more other types of seizures and implies a poor prognosis for the ultimate seizure control and

for normal mental development.9-11



Lennox-Gestaut Syndrome (L-G) is another classification of seizure disorder which has a peak age

of onset of four years.12 It is characterized by myoclonic and atypical absence seizures, regression of



intellectual functions and generalized spike wave discharges on the EEG at a rate below what is seen in

petit mal seizures. Several hundred attacks may occur in a day and multiple injuries from falls are

common. Diffuse cerebral atrophy is seen in 60% of cases.8



MEDICAL TREATMENT

The descriptive classifications above are important for determining the most appropriate medical

treatment. When patients have recurrent seizures, medication is prescribed until there have been no

seizures for at least four years. Epileptic patients are advised to avoid situations that could be dangerous or

life-threatening during seizures.1



All doctors must be aware of a condition called status epilepticus which is the rapid succession of

seizures so that the next seizure begins before the previous one has ended. Status epilepticus is a medical

emergency since continuous epileptic activity can damage the brain permanently. Of course death may

occur during a seizure if the patient aspirates contents of the stomach which either occlude airways or

prevent adequate oxygenation.8



When patients have been seizure free for at least four years withdrawal of medication may be

considered. There is unfortunately no way of predicting which patients can be managed without treatment.

Recurrence of attacks is most likely in patients who initially fail to respond to therapy, those with

convulsive jerking movements, those with multiple types, and those with continuing EEG abnormalities.1



HISTORY

Patient E is a five year old white female, who was small at birth and born breech. During her first

three years of life she had many viral infections and repeated attacks of otitis media. Some concern was

expressed by her mother over growth and language retardation. At age 13 months, however, psychomotor

skills had been assessed as normal.

At the age of 4 years 8 months, in October 1988, Patient E was playing as a day care center, when

she struck her head on the underside of a table. Within two hours her first grand mal seizure occurred.

Patient E’s second seizure occurred within three weeks.

Patient E was evaluated at the Mayo Clinic and was experiencing 10 to 30 seizures per day with

no seizure-free days. (Figure 1 is a graph prepared from Patients E’s daily seizure journal kept by her

parents. The recorded the number, time, type and severity of each seizure.) Seizure types were described as

being tonic, clonic, akinetic, and grand mal. The diagnosis of Lennox-Gestaut Syndrome was made. The

patient was described as being able to speak only a few intelligible phrases. She was tremulous, and had

difficulty standing.

Various laboratory tests were performed including a complete blood count, serum ammonia and an

SMA 20 and all were within normal ranges. A CT scan and MRI were negative for fractures and

pathologies. The EEG, however, showed a slow spike-wave abnormality as well as other features which

may occur in Lennox-Gestaut syndrome. The prognosis was determined to be grave and the comment was

made that the L-G syndrome is fraught with nearly uniform disappointment since medical therapy has very

few beneficial results.

Patient E was given Depakote, Zarontine, and ACTH therapy. Each was given singly and then

discontinued due to Patient E’s unusual or aggressive behavior. Finally, Tegretol/carbamazepine seemed to

have some positive effects on the grand mal type seizures. It was after this, however, that Patient E began

to have drop attacks.

On July 18, 1989 Patient E entered into a team evaluation and treatment plan at the Palmer

Chiropractic Clinic. At that time, Patient E was having 30 to 70 seizures per day. {Figure 1] Patient E

presented with a helmet, faceplate, and harness for protection against falls.

The patient’s communication skills were retarded. Physician exam revealed a waxy buildup in the

ears so that the TM could not be visualized. Neurological exam revealed the presence of hyper reflexive

and asymmetric reflexes. Orthopedic evaluation was unremarkable.

Further chiropractic evaluation revealed paravertebral muscular spasm in the cervical area;

cervical ROM severely restricted especially in the right lateral bending; right leg deficiency of 􀀁 to 1 inch;



suspected cervical misalignment resulting in an atlas subluxation complex.

A specific upper cervical x-ray series was taken.13,14 During patient placement for the nasium



view, certain postural deviations were noted. When asked to sit up straight, Patient E’s head, cervical, and

upper thoracic spine would not center directly over the pelvis and demonstrated excursion into the frontal

plane. No pathologies were noted on the x-rays.

Chiropractic x-ray analysis revealed a misalignment of the occipito-atlanto-axial region. Figure 2

is a representation of a radiograph showing Patient E’s misalignment in the frontal plane view. Rotation of

atlas in the transverse plane was also measured, but was minimal.

To correct the subluxation, Patient E was placed on the adjustment table side posture with the C1

transverse process as the contact point. An adjusting force was introduced to the spine using specific upper

cervical adjusting procedures.15 The success of the adjustment was measured by lessening of leg disparity,



increase of pelvic resistance, postural changes, and finally post adjustment x-ray analysis.

Patient E was adjusted on three consecutive days. After the first adjustment, Patient E’s right leg

changed from one inch deficiency to no noted deficiency.16 The patient began to rub her eyes and seemed



drowsy after the adjustment. The seizure pattern remained quite high that day. On the second day, the preadjustment

leg deficiency was 1/4th inch on the right. After the adjustment, the legs were even and the



pelvic resistance on the right was stronger that the day before. The adjustments were always made between

9:00 am and 1:00 pm. After 1:00 pm on the second day, Patient E had no more seizures during the day.

On the third and final day of care at the Palmer Chiropractic Clinic, the leg deficiency was 1/8th inch.



Again, after the adjustment, the legs were even, and the pelvic resistance was equal bilaterally. Patient E

had no further seizures after 1:00 pm on this day. The parents of Patient E commented that she was

showing more energy and more stability when standing. A postural change was quite evident when Patient

E was prepared for the post x-ray series. When instructed to sit up straight, Patient E’s head and upper

spine were centered over her pelvis. The vertical centering lines on the bucky were used for comparison.

Post x-ray analysis revealed a 91% reduction of the misalignment factors with all structures centered on the

vertical axis.

The parents had been counseled that after an adjustment they could expect exacerbations or

changes in symptomatology on the 3rd, 7th, 14th, and 28th day.17 On the 17th day after the adjustment

procedure, the seizures numbered almost 100 (more than ever before). On the 27th day, the seizures abated.



[Figure3] The seizures remained absent for approximately four weeks. The carbamazepine dosage was not

changed during this period.

At the time of this report, the dosage had been reduced by almost one half for the past two weeks.

Patient E has had six or fewer seizures per day. The seizures are completely absent on some days. After

fewer than 60 days of chiropractic care Patient E has been speaking with five or six word sentences. A

current speech evaluation is pending from her therapist and our patient has not been adjusted since July

1989. At re-evaluation, Patient E had no leg deficiency and her condition continues to improve.

DISCUSSION

The authors could find little chiropractic literature pertaining to epilepsy or seizure disorders.

Young reported on three cases which responded to chiropractic care.18 IN the medical articles reviewed on



this subject, little hope, if any, is expressed for the control or cessation of childhood seizures of this type.

Using statements like “woefully”, “poor diagnosis”, “retractability to treatment”, “fraught with uniform

disappointment”, and “grim foreboding”,2 this literature demonstrates the need for research no only in



alternative methods of treatment, but also research into possible causative factors as well.

The remission of Patient E’s epilepsy is a phenomenon whose timing is shortly preceded by the

adjustment procedure. Perhaps not all seizure disorders can be helped with spinal adjustments. However,

chiropractic care would surely be the most conservative treatment in the primary care system. Careful

investigation into each case may reveal possible avenues that may eventually help the patient reduce or in

some cases entirely eliminate the need for drug therapy.

ACKNOWLEDGEMENTS

The authors wish to acknowledge George Hess, D.C., Chris L. Hendricks, D.C., Vern Hagen,

D.C., and Dale Strama, D.C. for their part in the care of Patient E and Alana Ferguson, M.S., Susan Larkin,

D.C. and David Guerriero for help in manuscript preparation.

REFERENCES

1. Schroeder SA, Krupp MA, Tierney LM. Current medical diagnosis and treatment. Norwalk,

CT:Appleton & Lang; 1988: 576-580.

2. Snead OC III. Epilepsy in children, a practical approach. Seminars in Neurolgoy 1988; 8(1):24-

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3. Allen RB. Nutritional aspects of epilepsy. International Clinical Nutrition Review 1983; 3(3):3-

10.

4. Recent advances in childhood epilepsy. 17th International Epilepsyn Congress. Epilepsia 1988;



29 Supplements 3:S1-S24.

5. Sun JY. An analysis of the causes of epilepsy in 440 cases. Chung Hua Shen Ching Ching Shen

Ko Tsa Chih 1988 June; 21(3):141-4.

6. Crowell GF, Roach ES. Pyridoxine-dependent seizures. Am Fam Physician 1983; 27(3): 183-

187.

7. Harvey AM, Johns RJ, McKusick VA, Owens AH, Ross RS. Principles and practice of medicine.

Norwalk, CT; Appleton-Century-Croft; 1984:1236

8. Andreoli TC, Carpenter CCJ, Plum F, Smith LH Jr. Cecil essentials of medicine. 2d.ed.

Philadelphia: W.B. Saunders; 1990.

9. Evans OB, Hanson RR, Snead OC. The primary generalized epilepsies of childhood. Semin

Neurol 1988 Spring; 8(1):12-21.

10. Pazzaglia P et al. Drop attacks: an ominous change in the evolution of partial epilepsy.

Neurology 1985; 35: 1725-30.

11. Markland ON. Slow spike-wave activity in EEG and the associated clinical features; often called

Lennox-Gastaut Syndrome. Neurology (Minneap) 1977;27:746-757.

12. Laidlaw J, Richens A, Oxley J (eds). Textbook of epilepsy. 3d ed. New York; Churchill

Livingstone 1988.

13. Gregory RR. The NUCCA course: adjusting the atlas subluxation complex. Monroe, MI:

National Upper Cervical Association Inc. 1988.

14. Dickholtz M. Patient alignment for upper cervical x-rays. Upper Cervical Monograph 1980;

2(8):2-7.

15. Gregory RR. The NUCCA course: adjusting the atlas subluxation complex. Monroe, MI:

National Upper Cervical Association Inc. 1988.

16. Gregory RR. Biomechanics of C1 subluxation production. Upper Cervical Monograph 1988;

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17. Gregory RR. Post-adjustment healing cycle: nerve and tissue repair. NUCCA Educational

Conference, May 1979, unpublished seminar notes.

18. Young G. Chiropractic success in epileptic conditions. ACA Journal of Chiropractic 1982;

19(4):62-63.


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