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PubMed1990

Double-crush nerve compression in thoracic-outlet syndrome.

We studied 165 cases of thoracic-outlet syndrome in 142 patients in whom resection of the first rib had been performed. In seventy-three cases (44 per cent), there was compression of a nerve distally, as shown by electromyography and conduction studies. The most common secondary compression was carpal tunnel syndrome (forty-one cases). Thirteen patients needed an operation at three sites or more. Our results show that proximal compression of a nerve lessens its ability to withstand more distal compression. Once the diagnosis of thoracic-outlet syndrome has been made, the possibility of an additional distal compression neuropathy should be investigated.

Adolescent↗

PubMed1989

Nerve compression syndromes of the lower extremity.

Nerve compression syndromes of the lower extremity present a challenge in differential diagnosis. Compression of the common peroneal nerve occurs relatively frequently; compression of the sciatic nerve occurs infrequently. The pattern of weakness helps distinguish lumbar root entrapment from peripheral compression syndromes. Compression syndromes must also be differentiated from diabetic, alcoholic or vasculitic neuropathy. Recovery correlates with the degree and duration of nerve injury. Thus, early diagnosis and treatment are important.

Diagnosis, Differential↗

PubMed1989

Changes in noradrenaline and histamine in monkey spinal cords traumatised by weight drop, compression and subsequent decompression.

Levels of noradrenaline (NA) and histamine (H) in the spinal cord of monkeys at 8, 24 and 48 hr following 200 g/cm contusion injury, 50 g of compression injury at 8 hr and decompression for 16 and 40 hr following 8 hr of compression were studied in the traumatised and in an adjacent non-traumatised segment. The NA level doubled in the traumatised and non-traumatised segments at 8 hr contusion injury followed by a slow decline to control values at 24 and 48 hr of contusion injury. There was no change in NA content of the spinal cord segments at 8 hr of compression injury. Decompression for 16 hr following 8 hr of compression increased NA content of the traumatised segment. H levels decreased in the traumatised and non-traumatised segments at 24 and 48 hr of contusion injury. Compression for 8 hr elevated H in the traumatised and non-traumatised segments. On decompression H level was further increased in the traumatised segment.

Animals↗

PubMed1985

[Changes of microcirculation dynamics in the formation of edema following spinal compression injury in rabbits].

The changes in microcirculation dynamics were investigated, after giving acute compression to the spinal cord in rabbits. When the 8th thoracic cord was compressed for one minute with a plummet weighing 50g, paraparesis occurred, from which the animals could recovered within two weeks. The blood flow at the compressed region, determined by the hydrogen clearance method, one hour after the injury was increased to 154% of the pre-injury level, while the flow was reduced by 22% six hours later. The vascular permeability, estimated by the fluorescein method, was found to be 3.3 times greater in the injured animals than that in controls only at one hour after compression. The water contents of the spinal cord, determined by the dry weight method, were gradually increased up to six hours. These results suggest that vasogenic edema due to the primary damage to the vascular system in the spinal cord may occur within one hour of the compression and cytotoxic edema may appear six hours later.

Animals↗

PubMed1979

[Neurovascular compression syndroms of the shoulder girdle (author's transl)].

Shoulder girdle compression syndroms appear intermittently and according to body carriage. Very seldom they are caused by neck ribs, mostly by a costoclavicular narrowness. Important for the symptoms is the nerval plexus compression, for diagnostic reasons the blood vessel compression. Essential are provocating tests, subclavia phonogramms and in doubtful cases, angiography. Oszillo- and sonography often fail, EMG and nerval conductive measurement are only of differential diagnostik importance. In all together 120 healthy persons compression was shown phonographically, phlebographically and manometrically in 58--88%. Only the symptomatic and distinct compression are abnormal. Physiotherapy should be applied, only operative decompression is a causal treatment. The transaxilar resection of the first rib with scalenotomy and eventually also resection of a neck rib is by fat better than any other method. This is a report of 112 operated patients.

Angiography↗

PubMed1984

Peripheral nerve compression by brachial artery-basilic vein vascular access in long-term hemodialysis.

This report presents the first description of direct peripheral nerve compression as a complication of brachial artery-basilic vein vascular access in patients with uremia who are receiving long-term hemodialysis. Three patients are presented. An expanding basilic vein hematoma compressed the radial nerve in one patient. A graft associated abscess adjacent to the brachial artery compressed the median nerve in a second patient. A basilic vein aneurysm compressed the median nerve in a third patient. In two cases, electrodiagnostic studies were helpful in identifying the location and severity of the peripheral nerve dysfunction, and in excluding more common distal nerve dysfunction, which is sometimes seen in these patients as a result of circulatory alterations in the extremity caused by dialysis. Prompt surgical decompression led to significant recovery of nerve function in all three patients. It is concluded that direct peripheral nerve compression is a rare complication of brachial artery-basilic vein vascular access in patients with uremia who are receiving long-term hemodialysis.

Adult↗

PubMed1984

[Spinal cord compression in malignant plasmacytic diseases. Apropos of 6 cases].

Myeloma may be complicated or revealed by spinal cord compression. Out of 105 cases of myeloma admitted to this Department, 6 cases of spinal cord compression were observed, with a favourable outcome after treatment by laminectomy combined with radiotherapy. In 5 cases out of 6, spinal cord compression was either the presenting sign or occurred within the first months after diagnosis. Compression occurred in the thoracic cord in 5 cases, and in the lumbar cord in 1 case. The interval between the first symptom and diagnosis varied greatly (from a few hours to 1 year), as did the degree of paraplegia, which ranged from paraparesis to flaccid paraplegia. A favourable outcome occurs in most other reported cases, in contrast with spinal cord compression from metastases. Treatment (laminectomy-radiotherapy or both) remains controversial.

Adult↗

PubMed1982

Compression neuropathy.

Some of the experimental, pathologic, and clinical features of extremity compression are reviewed with special reference to vulnerability of peripheral nerves to compressive forces at specific anatomic locations. Attention is directed toward syndromes resulting from mechanical factors, and it should be pointed out that a nerve can be compressed at more than one level. Localized peripheral nerve compression is common in clinical medicine; carpal tunnel syndrome is the most common example. Physicians who maintain a high index of suspicion to the signs and symptoms of peripheral nerve compression will diagnose and treat these conditions earlier and thereby reduce the number of patients who develop permanent functional disabilities.

Axilla↗

PubMed1995

[Medulla oblongata compression by tortuous vertebral artery: case report].

We reported a case of a 58-year-old woman who suffered from progressive tetraparesis and sensory disturbance caused by compression of the medulla oblongata brought about by bilateral tortuous vertebral arteries. The neurological examination on admission revealed tetraparesis, sensory disturbance in all modalities below the level of C2, onion-skin pattern sensory disturbance of the face, and motor weakness of the sternocleidomastoid muscles. X-ray films of the cervical spine showed OPLL at the level of C2.3, but on MRI the dural theca was not seen to be compressed at that level. MRI and vertebral angiography demonstrated ventrolateral compression of the medulla oblongata by bilateral tortuous vertebral arteries. After suboccipital craniectomy and C1.4 laminectomy, decompression of the medulla oblongata was performed. Both vertebral arteries were compressing the medulla oblongata at the ventrolateral side. Transposition of the vertebral arteries seemed impossible due to perforating branches to the medulla. After section of the dentate ligaments at C1 level, the medulla oblongata was decompressed and moved backward. Some small pieces of Dacron were inserted between the arteries and the medulla, in order to decrease the pulsatile effect of the vertebral arteries. Postoperatively, the patient's tetraparesis and sensory disturbance gradually improved. There are 6 reported cases concerning compression of the medulla oblongata by the vertebral artery. As MRI becomes more frequently used in neurological situations, it is important to keep the presence of such an entity in mind.

Female↗

PubMed1994

Effect of the 21-aminosteroid U74006F and methylprednisolone on motor function recovery and oedema after spinal cord compression in rats.

The effect of the 21-aminosteroid U74006F and methylprednisolone (MP) on motor function and oedema were investigated after spinal cord compression in rats. Each compound was administered i.v. as a single dose 60 min after injury. The hind limb motor function was assessed using the inclined plane technique and expressed as the capacity angle. The water content was calculated as the percent wet weight of the total weight. Prior to compression the capacity angle was close to 62-64 degrees. One day after compression the motor function was reduced significantly in all rats. However, the capacity angle was significantly higher after treatment with U74006F or MP than with vehicle, i.e. 50 degrees +/- 4, 45 degrees +/- 5, and 32 degrees +/- 3, respectively. This improved functional recovery persisted during the initial nine days. After compression of the spinal cord the water content increased to a maximum on day 4 in all groups. The water content was not significantly different in any of the groups except on day one and nine when it was less in groups treated with U74006F. In conclusion, a single i. v. injection of U74006 or MP given 60 min after compression of the spinal cord improved motor function without effecting oedema expressed as water content.

Animals↗

PubMed1993

Usefulness of motor evoked potentials in compressive myelopathy.

Motor Evoked Potentials elicited by transcranial magnetic stimulation were recorded from 1 degree Dorsal Interosseus for the upper limbs and from Extensor Digitorum Brevis for the lower limbs in 42 subjects with compressive myelopathy (36 in the cervical region and 6 in the dorsal region), radiologically defined by Nuclear Magnetic Resonance (NMR) imaging, with no clinical and radiological signs of radiculopathy. Central motor conduction abnormalities in the cortex-C8 and cortex-L5 tract were compared with clinical signs of motor impairment and with NMR findings. The subjects with medullar hyperintensity of NMR signal at the compression site level, showed a central conduction time (C.C.T.) prolongation in at least one side in the 70% of cases in the cortex-C8 tract and in the 95% of cases in the cortex-L5 tract, while in the cases with no compression site alterations of signal, C.C.T. abnormalities were observed only in 25% in the cortex-C8 tract and in 42% in the cortex-L5 tract. In 12 subjects (10 with cervical compression and 2 with dorsal compression) we compared Motor Evoked Potentials before, two weeks and two months after surgical decompression. The C.C.T. cortex-C8 and cortex-L5 improved at least in one side in 11 out of the 12 subjects, showing a good correlation with clinical recovery. In the examined patients we found a latency reduction statistically significant between the first and second investigation, with a trend to stabilization in the following controls.

Adult↗

PubMed1996

MR screening for brain stem compression in hypertension.

PURPOSE: To determine the clinical usefulness of MR imaging to screen for vascular compression of the lateral medulla, considered by some to be responsible for neurogenic hypertension. METHODS: MR images and clinical records of 120 adults who had received brain MR imaging for any reason were divided into two groups: group 1 (n = 60) consisted of patients with essential hypertension and group 2 (n = 60) included patients who lacked a diagnosis of hypertension. No patient manifested symptomatic cranial neuralgias. The root entry zone of cranial nerves IX and X into the left lateral medulla was examined by MR imaging for proximity to the ipsilateral vertebral artery or its branches. Images lacking any contact between visible vascular structures and the root entry zone were recorded as normal. Vascular compression was graded according to the degree of proximity to the root entry zone. Lateral medullary contact only (grade I), contact and depression (grade II), or lower brain stem displacement or rotation (grade III) of the root entry zone were recorded in both hypertensive and normotensive patients. Among hypertensive patients, additional data were gathered from electrocardiographic, echocardiographic, and urinary protein reports. RESULTS: We found compression in 34 (57%) of the patients from group 1 and in 33 (55%) of the patients from group 2. Compressions in group 1 were grade I in 22 (37%) of the patients, grade II in 8 (45%), grade II in 4 (7%), and grade III in 2 (3%). There were no statistically significant differences in MR findings between the two groups. Among group 1 patients, MR grading did not predict end-organ changes in the heart (left axis deviation and left ventricular hypertrophy) or kidneys (proteinuria). CONCLUSION: Vascular compression of the root entry zone of cranial nerves IX and X into the left lateral medulla is not an adequate lesion to produce systemic hypertension. This finding is as common among normotensive patients as among hypertensive populations. Neither the presence nor the severity of changes in the root entry zone on MR images increases the occurrence of common end-organ responses in the heart or kidneys among hypertensive patients. MR screening is not warranted among hypertensive patients lacking symptomatic cranial neuralgias.

Adult↗

PubMed1998

[Cervical myelopathy caused by bilateral vertebral artery compression].

We report a rare case of myelopathy caused by compression of the upper cervical cord by the bilateral anomalous vertebral arteries. A 49-year-old man had dragged his right foot for 4 years. He also complained of a tingling sensation in his right arm and occipitalgia. Neurological examination disclosed right hemiparesis, hypalgesia in the right half of the body and hypertonicity of the lower extremities. MRIs showed a flow void area which compressed and distorted the spinal cord bilaterally at the level of the atlas. A vertebral angiogram showed that the bilateral vertebral arteries had pierced the dura matter under the posterior arch of the atlas, turned upward and laterally in the vertebral canal, making vascular loops at the level of the atlas. 3D CT angiography showed the loops convex medially in the anterior part of the vertebral canal. With these findings, we diagnosed the patient as suffering compression of the cervical cord by the bilateral anomalous vertebral arteries. Suboccipital craniectomy and C1 laminectomy were performed. When the dura mater was opened, the dorsolateral aspect of the spinal cord was found to be compressed and indented markedly by the vertebral arteries. To decompress the spinal cord, the vertebral arteries were retracted dorsolaterally by means of Gore-tex tape and anchored to the spinous process of the axis. Postoperatively, his neurological symptoms improved. Postoperative MRIs showed that the spinal cord was decompressed and had recovered its contour. A review of the literature revealed that only 3 such cases as this one have been reported. The clinical features of these rare cases are nonspecific myelopathy and concomitant occipitalgia or neck pain. The main cause of this rare entity seemed to be the compression of the vertebral artery through its course when it enters the vertebral canal between the atlas and the axis.

Humans↗

PubMed1998

Study of spinal cord evoked injury potential by use of computer modeling and in dogs with naturally acquired thoracolumbar spinal cord compression.

OBJECTIVE: To add objective measurements of the characteristics of evoked injury potentials (EIP) and their relations to clinical severity in dogs with thoracolumbar spinal cord damage. ANIMALS: 25 dogs with naturally acquired spinal cord compression attributable to disk extrusion or vertebral fracture at the level of the thoracolumbar junction and with various degrees of paresis/paralysis. PROCEDURE: Spinal cord potentials evoked by tibial nerve stimulation were recorded every 5 to 10 mm at the lamina level in the vicinity of the cord compression. This allowed an EIP to be recorded even in the least handicapped dogs. A computer model yielded information about the waveform changes of the EIP in the vicinity of conduction blocks. RESULTS: The EIP waveform changed from biphasic to monophasic a short distance caudad to the location of spinal cord compression. Location of a maximal conduction block was measured in relation to position of the electrodes recording this waveform change. The distance between the assumed conduction block and the actual spinal cord compression was larger in the most affected dogs. The amplitude of the EIP was not related to severity of the clinical picture; however, the proximity of the recording electrode to the spine influenced the amplitude and the waveform of the EIP. CONCLUSION AND CLINICAL RELEVANCE: Change in the EIP waveform from biphasic to monophasic makes it possible to estimate the conduction block location along the spinal cord. A large distance between the assumed conduction block and site of actual cord compression could be an objective argument to confirm severity of a lesion.

Animals↗

PubMed1998

[Vascular compression and cranial nerve diseases].

This paper offers a review of cranial nerve rhizopathies caused by vascular compression of cranial nerves in the posterior cranial fossa. We present our results of microvascular decompression for trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia caused by compression of the 5th, 7th and 9th cranial nerves, respectively. After a median observation time of 38 months, 20 of 25 patients with trigeminal neuralgia were completely free of pain, and one patient reported more than 50% pain relief. Four out of five patients treated for hemifacial spasms were completely free of spasms. Of two patients treated for glossopharyngeal neuralgia, one reported complete pain relief, whereas the other reported less than 50% pain relief. No serious complications occurred. The results of microvascular decompression reported in the literature reviewed, including results of the treatment of tinnitus and positional vertigo due to compression of the 8th cranial nerve, hypertension due to compression of the 10th cranial nerve and spastic torticollis due to compression of the 11th cranial nerve. It is concluded that the rationale behind microvascular decompression is supported by an extensive amount of data.

Adult↗

PubMed1978

Correlation of spinal cord blood flow and function in experimental compression.

Focal spinal cord blood flow was measured in the left dorsal column of monkeys' spinal cords at T6 during slow balloon compression of the same segment. The physiological integrity of the spinal cord was monitored by the recording of the summated spinal evoked response (SER). In all cases, the evoked response did not disappear until the blood flow in the compressed segment was zero. In four animals, a definite phase of hyperemia occurred during compression, at which time the amplitude of the evoked response was reduced. A post-ischemic hyperemia occurred in seven animals. The evoke response returned in all animals to a varying degree within one-hour post-deflation. The results suggest that mechanical forces of compression, rather than ischemia, are mainly responsible for the loss of neural conduction in such a model. If ischemia plays a role at all in the loss of function in such a model, it appears that focal ischemia secondary to compression in the spinal cord must be profound for loss of physiologic function to occur.

Animals↗

PubMed1976

[Radial nerve compression].

A new compression syndrome of the deep branch of the radial nerve is described, in which a sudden anterior displacement of a part of this nerve under maximal tension is followed by an axonotmesis. This happens in an area in which the deep branch of the radial nerve crossed some narrow structures which are unyielding and have more compression strength (tense cords of connective tissue Fig. 3). The operative finding of a torsion of the injured fascicles justifies the correctness of the immediate operative revision; otherwise the nerve regeneration would be impaired by the torted empty endoneural tubes. This description is a further constribution not observed before to the compression syndromes of the radial nerve, since in 1970 the author was able to give an explanation for the pathogenesis of compression palsies of the radial nerve, unclear up to that time but observed after forceful muscle contractions again and again since the beginning of this century. This observation gives the evidence that the occurrence of a peripheral compression lesion of nerves is not bound absolutely on the existence of a "physiological narrowness" (fibrous or osteofibrous tunnel etc.). This is also true for the median nerve.

Humans↗

PubMed1997

Coexisting peripheral nerve and cervical cord compression.

STUDY DESIGN: The authors investigated the clinical usefulness of recording motor evoked potentials after transcranial magnetic stimulation in coexisting peripheral nerve and cervical cord lesions. OBJECTIVE: To show that the measurement of central motor conduction time from the abductor policis brevis and the abductor digiti minimi can be used as a good screening method for double lesions involving peripheral nerves and the cervical cord. SUMMARY OF BACKGROUND DATA: Transcranial magnetic stimulation has been used in the diagnosis of compressive cervical myelopathy. This technique could be useful in the assessment of patients with an entrapment neuropathy and cervical myelopathy. METHODS: Motor evoked potentials after transcranial magnetic stimulation, compound muscle action potentials, and F waves after supramaximal peripheral nerve stimulation were recorded from the abductor policis brevis and the abductor digiti minimi. The central motor conduction time was calculated by subtracting the peripheral conduction time from the motor evoked potentials latency. RESULTS: Ten patients with coexisting peripheral nerve and cervical cord lesions were evaluated. Two patients did not show satisfactory improvement after the decompression of the entrapment lesions, and six patients had hyperreflexia of lower limbs. In seven of these patients, the central motor conduction time was prolonged an average of 2.5 standard deviation of the normal value. The remaining two patients had spinal cord compression due to the ossification of the posterior longitudinal ligament. The spinal cord compression was demonstrated by magnetic resonance imaging, but the central motor conduction time was normal. Subjective symptoms improved in these two patients after decompressive surgery at the entrapment site alone. CONCLUSIONS: Measurement of the central motor conduction time using motor evoked potentials is an ideal diagnostic approach for patients with coexisting entrapment neuropathy and cervical cord compression.

Carpal Tunnel Syndrome↗