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A Man with a Neuropathy, Weight Loss, and Lung Nodules
Case 64
A Man with a Neuropathy, Weight Loss, and Lung Nodules
A 31-year-old black man was referred from another institution for evaluation of a neuropathy with a nerve biopsy suggestive of vasculitis. He had been healthy until 1 year before when he developed perioral dysesthesias followed by hand and leg weakness, with numbness in the legs and difficulty walking. He had a 60-pound weight loss. Previous workup revealed normal erythrocyte sedimentation rate and a spinal fluid protein of 60 mg/dL without cells. FANA was negative. A chest x-ray showed multiple pulmonary nodules. Past medical history was unremarkable. His father had some type of lung disease, apparently chronic obstructive pulmonary disease, and was a non–insulin dependent diabetic. The patient drank a six-pack of beer per month, but did not smoke. He appeared cachetic but had no visceromegaly or palpable nodes. Mentation and cranial nerves were normal except for decreased sensation in the right mental area and he had facial asymmetry from mild weakness of the right hemiface. There was weakness of the hand interossei muscles and bilateral foot drop with prominent weakness of the distal muscles in both legs. He had areflexia in the legs and arms, vibration sense was absent in the toes and ankles and decreased in the knees and toes, and there was decreased pinprick and touch sensations up to the
midarm and up to the midcalf. The ulnar nerves were thick. Complete blood count and metabolic panel were normal. Antineutrophilic cytoplasmic antibody titers were normal. A spinal fluid test showed 7 white blood cells, 97% lymphocytes, and 3 monocytes; cytology was negative for malignant cells, protein was 678 mg/dL. Acid-fast bacilli and fungus cultures were negative. Electrophoresis, human T-lymphotropic virus 1, and HIV tests were negative. Angiotensin-converting enzyme was elevated at 69 U/Lt (normal, <52 U/Lt). He had a steppage gait.
WHAT IS THE DIFFERENTIAL DIAGNOSIS? This patient had pulmonary nodules and a peripheral neuropathy. The differential diagnosis includes sarcoidosis, particularly as the angiotensin-converting enzyme was mildly elevated, but there was no evidence of a mediastinal mass. Another possibility is Wegener’s granulomatosis which presents with peripheral neuropathy and granulomatosus lesions in the lungs. A malignant lymphoma and lymphoid granulomatosis could have a similar presentation. Tuberculosis does not cause a neuropathy; leprosy does not present with lung disease.
AN EMG TEST WAS PERFORMED Motor Nerve Studies
Motor Nerve Studies—cont’d
Nerve and Site
Latency (ms)
Amplitude (mV)
Conduction Velocity (m/s)
Peroneal Nerve R.
Normal £ 5.7
Normal ≥3
Normal ≥ 40
NR NR
NR NR
— NR
Tibial Nerve L.
Normal ≥ 5.3
Normal ≥4
Normal ≥ 50
Ankle Pop. fossa
6.3 NR
0.5 NR
— NR
Ankle Fibular head
Nerve and Site
Latency (ms)
Amplitude (mV)
Conduction Velocity (m/s)
Median Nerve L.
Normal £ 4.2
Normal ≥6
Normal ≥ 50
3.1 8.4
16 12
— 58
Normal £ 3.6
Normal ≥8
Normal ≥ 50
4.2 9.4 12.8
3 3 3
— 44 35
Wrist Elbow Ulnar Nerve L. Wrist Below elbow Above elbow
411
412
Case 64
F-wave Studies Nerve Median nerve L. Ulnar nerve L.
Latency (ms)
Normal Latency £ (ms)
27.6 30
30 30
Sensory Nerve Studies
Nerve Median nerve L. Ulnar nerve L. Sural nerve R.
Onset Latency (ms)
Normal Onset Latency £ (ms)
Peak Latency (ms)
Normal Peak Latency £ (ms)
Amp (mV)
Normal Amp ≥ (mV)
Conduction Velocity (m/s)
Normal Conduction Velocity ≥ (m/s)
2.4 NR NR
2.6 2.6 3.5
2.9 NR NR
3.1 3.1 4.0
17 NR NR
20 13 11
54 NR NR
50 50 40
EMG Data Muscle
Insrt Activity
Fibs
Pos Waves
Fasc
Amp
Dur
Poly
Pattern
Biceps brachii L. Flexor carpi radialis L. Flexor carpi ulnaris L. Extensor digitorum com. L. 1st dorsal interosseus L. Vastus lateralis L. Tibialis anterior L. Gastrocnemius L. Gastrocnemius R.
Norm Norm Inc Norm Inc Norm Inc Inc Inc
None None None None None None None None None
None None None None 1+ None 1+ 1+ 1+
None None None None None None None None None
Norm Norm Lg Norm Lg Lg Lg Norm Norm
Norm Norm Inc Norm Inc Inc Inc Norm Norm
None None None None None None None None None
Full Full Full Full Red Full Red Red Red
WHAT WERE THE EMG FINDINGS?
WHAT SHOULD BE DONE NEXT?
The test showed peripheral neuropathy involving some nerves and sparing others. There were no recordable CMAPs from the tibial or peroneal nerve stimulation; there was slowing of the ulnar nerve conduction velocity with low-amplitude CMAP, but the median nerve was normal. The F-responses were normal. SNAPs were absent in the ulnar and sural nerves. There was diffuse denervation and reduced motor unit recruitment in the legs. It was concluded that he had a neuropathy with axonal degeneration, with features of a mononeuritis multiplex despite the apparent symmetrical clinical distribution of finding in the limbs. A CAT scan of the chest revealed multiple pulmonary nodules (Fig. 64-1A); lung biopsy showed granulomatous lymphocytic infiltrates with some hemorrhage (see Fig. 64-1B and C). The cells had irregular nuclei. There were both B and T lymphocytes, but mainly T-cells. They appear malignant but a flow cytometry revealed no clear clonicity. Bone marrow biopsy showed similar findings.
The sural nerve biopsy was reviewed and showed evidence of axonal degeneration with lymphocytic infiltrations in the perineural area, some around vessels (see Fig. 64-1D). In some areas, the endoneurium was also infiltrated. The patient was treated with cyclophosmamide which produced remission. Eight months later, he became progressively worse and had multiple organ involvement with lymphocytic infiltrates. He did not respond to aggressive chemotherapy and died. No autopsy was performed.
DISCUSSION This patient had multinodular infiltration of the lungs that appeared to be caused by T-cell non-Hodgkin’s lymphoma that was not well categorized. He had a polyneuropathy, but some nerves were more affected than others, and the nerve biopsy showed pseudovasculitic infiltrates and also axonal degeneration. In
A Man with a Neuropathy, Weight Loss, and Lung Nodules
A
C
B
D
413
FIGURE 64-1 A, Contrast CAT scan of the chest showing multiple small nodes. B, Lung infiltrates consisting mostly of lymphocytes (H&E stain, ×100). C, Homogenous mononuclear cells in node (H&E stain, ×200). D, Perineural cellular infiltrate in sural nerve (toluidine blue stain, ×200).
some areas, the endoneurium was infiltrated by lymphoid cells. Lymphomas can cause various neurological manifestations, including peripheral neuropathies from a metabolic or infectious process or by paraneoplastic mechanisms and tumor infiltration.1 These include a sensorimotor polyneuropathy, Guillain-Barré syndrome (GBS) and a chronic inflammatory demyelinating polyneuropathy (CIDP), particularly in those with Hodgkin’s lymphoma.1–6 Other manifestations include cranial neuropathies, as in this patient; they could also cause radiculopathies from infiltration of the dura and adjacent nerves. Lymphomas can also cause plexopathies, mononeuropathies, and mononeuritis multiplex.7 Non-Hodgkin’s lymphoma is the most common cause of a lymphomatous neuropathy. Hodgkin’s lymphoma, on the other hand, can also manifest with an autoimmune neuropathy, such as GBS or CIDP. Other manifestations
of a lymphoma include vasculitis, cryoglobulinemia, motor neuron disorders, Isaacs syndrome and stiff-person syndrome.8–11 The term neurolymphomatosis defines a malignant lymphomatous infiltration of nerves causing their focal or diffuse enlargement.12–20 In this the cell types can be defined by flow cytometry and immunohistochemistry. The great majority are B cells; only about 10% represent T cells. Other lymphomatous diseases that affect the nervous system include intravascular B-cell lymphoma or malignant angioendotheliomatosis in which the lymphoma is confined to the lumen of vessels, and this can cause strokes, but sometimes also mononeuropathies.18 Lymphoid granulomatosis is an angiocentric non-neoplastic granulomatous disease associated with Epstein-Barr viral infection that could rarely manifest as a peripheral neuropathy.21,22
414
Case 64
Detailed evaluation on patients with proper diagnostic techniques, particularly bone marrow and lymph node biopsy, are useful in determining, if possible, the exact type of lymphoma for treatment.1
SUMMARY This patient had multiple lung nodules and a neuropathy. On EMG some nerves were more affected than others with axonal degeneration. He had a lymphomatous infiltration of the lungs and peripheral nerves. He initially responded to chemotherapy, but later he developed multiorgan involvement.
IMPORTANT POINTS • The differential diagnosis of patients with lung nodes and peripheral neuropathy includes sarcoidosis, infections, Wegener’s granulomatosis, lymphoid granulomatosis, and tumors, such as lymphoma. • Neurolymphomatosis refers to invasion of peripheral nerves and/or central nervous system lymphoma. • Lymphoma can manifest with polyneuropathy, mononeuropathies, plexopathies or radiculopathy, and, rarely, Guillain-Barré syndrome, chronic inflammatory demyelinating polyradiculoneuropathy and other autoimmune disorders (such as cryoglobulinemia), vasculitis, stiffperson syndrome, and Isaacs syndrome.
REFERENCES
6.
7.
8.
9.
10.
11.
12. 13.
14.
15.
16. 17. 18.
1. Kelly JJ, Karcher DS: Lymphoma and peripheral neuropathy: A clinical review. Muscle Nerve 31:301–313, 2005. 2. Baehring JM, Damek D, Martin EC, et al: Neurolymphomatosis. Neuronocol 5:104–115, 2003. 3. Croft PB, Urich H, Wilkinson M: Peripheral neuropathy of sensorimotor type associated with malignant disease. Brain 90:31–66, 1967. 4. Hunt WE, Bouroncle BA, Meagher JN: Neurological complications of leukemia and lymphomas. J Neurosurg 16:135– 151, 1959. 5. Germignani F, Melli G, Inglese C, Marbini A: Cryoglobulinemia is a frequent cause of peripheral neuropathy in undi-
19. 20. 21.
22.
agnosed referral patients. J Peripher Nerv Syst 7:59–64, 2002. Creange A, Theodorou I, Sabourin JC, et al: Inflammatory neuromuscular disorders associated with chronic lymphoid leukemia: Evidence for clonal B cells within muscle and nerve. J Neurol Sci 137:35–41, 1996. Rahmani M, Birouk N, Amarti A, et al: T-cell lymphoma revealed by a mononeuritis multiplex: Case report and review of literature. Rev Neurol (Paris) 163(4):462–490, 2007. Wada M, Kurita K, Tajima K, et al: A case of inflammatory demyelinating polyradiculoneuropathy associated with T-cell lymphoma. Acta Neurol Scand 107:62–66, 2003. Walk D, Handelsman A, Beckmann E, et al: Mononeuropathy multiplex due to infiltration of lymphoma in hematologic remission. Muscle Nerve 21:823–826, 1998. Ince PG, Shaw PJ, Fawcett PR, Bates D: Demyelinating neuropathy due to primary IgM kappa B cell lymphoma of peripheral nerve. Neurology 37:1231–1235, 1987. Lahrmann H, Albrecht G, Drlicek M, et al: Acquired neuromyotonia and peripheral neuropathy in a patient with Hodgkin’s disease. Muscle Nerve 24:834–838, 2001. Borit A, Altrocchi PH: Recurrent polyneuropathy and neurolymphomatosis. Arch Neurol 24:40–49, 1971. Diamond AL, Thomas FP: Neurolymphomatosis. Medlink: Clinical summaries. 2003. Available at www.medlink.com (retrieved April 14, 2004). Trelles JO, Urquiaga C, Palomino L, Trelles L: Human peripheral neurolymphomatosis (reticuloendothelial polyradiculoneuritis). J Neurol Sci 28:187–202, 1976. Diaz-Arrastia R, Younger DS, Hair L, et al: Neurolymphomatosis: A clinicopathologic syndrome re-emerges. Neurology 42:1136–1141, 1992. Gordon PH, Younger DS: Neurolymphomatosis. Neurology 46:1191–1192, 1996. Grisold W, Drlicek M, Jellinger K: Neurolymphomatosis. Neurology 43:1628–1629, 1992. Vital C, Heraud A, Vital A, et al: Acute mononeuropathy with angiotropic lymphoma. Acta Neuropathol (Berl) 78:105–107, 1989. Borit A, Altrocchi PH: Recurrent polyneuropathy and neurolymphomatosis. Arch Neurol 24:40–49, 1971. Baehring JM, Damek D, Martin EC, et al: Neurolymphomatosis. Neuro-Oncol 5:104–115, 2003. Bone RC, Vernon M, Sobonya RE, Rendon H: Lymphomatoid granulomatosis: Report of a case and review of the literature. Am J Med 65:709–716, 1978. Hogan PJ, Greenberg MK, McCarty GE: Neurologic complications of lymphomatoid granulomatosis. Neurology 31:619–620, 1981.
A Man with a Neuropathy, Weight Loss, and Lung Nodules
A 31-year-old black man was referred from another institution for evaluation of a neuropathy with a nerve biopsy suggestive of vasculitis. He had been healthy until 1 year before when he developed perioral dysesthesias followed by hand and leg weakness, with numbness in the legs and difficulty walking. He had a 60-pound weight loss. Previous workup revealed normal erythrocyte sedimentation rate and a spinal fluid protein of 60 mg/dL without cells. FANA was negative. A chest x-ray showed multiple pulmonary nodules. Past medical history was unremarkable. His father had some type of lung disease, apparently chronic obstructive pulmonary disease, and was a non–insulin dependent diabetic. The patient drank a six-pack of beer per month, but did not smoke. He appeared cachetic but had no visceromegaly or palpable nodes. Mentation and cranial nerves were normal except for decreased sensation in the right mental area and he had facial asymmetry from mild weakness of the right hemiface. There was weakness of the hand interossei muscles and bilateral foot drop with prominent weakness of the distal muscles in both legs. He had areflexia in the legs and arms, vibration sense was absent in the toes and ankles and decreased in the knees and toes, and there was decreased pinprick and touch sensations up to the
midarm and up to the midcalf. The ulnar nerves were thick. Complete blood count and metabolic panel were normal. Antineutrophilic cytoplasmic antibody titers were normal. A spinal fluid test showed 7 white blood cells, 97% lymphocytes, and 3 monocytes; cytology was negative for malignant cells, protein was 678 mg/dL. Acid-fast bacilli and fungus cultures were negative. Electrophoresis, human T-lymphotropic virus 1, and HIV tests were negative. Angiotensin-converting enzyme was elevated at 69 U/Lt (normal, <52 U/Lt). He had a steppage gait.
WHAT IS THE DIFFERENTIAL DIAGNOSIS? This patient had pulmonary nodules and a peripheral neuropathy. The differential diagnosis includes sarcoidosis, particularly as the angiotensin-converting enzyme was mildly elevated, but there was no evidence of a mediastinal mass. Another possibility is Wegener’s granulomatosis which presents with peripheral neuropathy and granulomatosus lesions in the lungs. A malignant lymphoma and lymphoid granulomatosis could have a similar presentation. Tuberculosis does not cause a neuropathy; leprosy does not present with lung disease.
AN EMG TEST WAS PERFORMED Motor Nerve Studies
Motor Nerve Studies—cont’d
Nerve and Site
Latency (ms)
Amplitude (mV)
Conduction Velocity (m/s)
Peroneal Nerve R.
Normal £ 5.7
Normal ≥3
Normal ≥ 40
NR NR
NR NR
— NR
Tibial Nerve L.
Normal ≥ 5.3
Normal ≥4
Normal ≥ 50
Ankle Pop. fossa
6.3 NR
0.5 NR
— NR
Ankle Fibular head
Nerve and Site
Latency (ms)
Amplitude (mV)
Conduction Velocity (m/s)
Median Nerve L.
Normal £ 4.2
Normal ≥6
Normal ≥ 50
3.1 8.4
16 12
— 58
Normal £ 3.6
Normal ≥8
Normal ≥ 50
4.2 9.4 12.8
3 3 3
— 44 35
Wrist Elbow Ulnar Nerve L. Wrist Below elbow Above elbow
411
412
Case 64
F-wave Studies Nerve Median nerve L. Ulnar nerve L.
Latency (ms)
Normal Latency £ (ms)
27.6 30
30 30
Sensory Nerve Studies
Nerve Median nerve L. Ulnar nerve L. Sural nerve R.
Onset Latency (ms)
Normal Onset Latency £ (ms)
Peak Latency (ms)
Normal Peak Latency £ (ms)
Amp (mV)
Normal Amp ≥ (mV)
Conduction Velocity (m/s)
Normal Conduction Velocity ≥ (m/s)
2.4 NR NR
2.6 2.6 3.5
2.9 NR NR
3.1 3.1 4.0
17 NR NR
20 13 11
54 NR NR
50 50 40
EMG Data Muscle
Insrt Activity
Fibs
Pos Waves
Fasc
Amp
Dur
Poly
Pattern
Biceps brachii L. Flexor carpi radialis L. Flexor carpi ulnaris L. Extensor digitorum com. L. 1st dorsal interosseus L. Vastus lateralis L. Tibialis anterior L. Gastrocnemius L. Gastrocnemius R.
Norm Norm Inc Norm Inc Norm Inc Inc Inc
None None None None None None None None None
None None None None 1+ None 1+ 1+ 1+
None None None None None None None None None
Norm Norm Lg Norm Lg Lg Lg Norm Norm
Norm Norm Inc Norm Inc Inc Inc Norm Norm
None None None None None None None None None
Full Full Full Full Red Full Red Red Red
WHAT WERE THE EMG FINDINGS?
WHAT SHOULD BE DONE NEXT?
The test showed peripheral neuropathy involving some nerves and sparing others. There were no recordable CMAPs from the tibial or peroneal nerve stimulation; there was slowing of the ulnar nerve conduction velocity with low-amplitude CMAP, but the median nerve was normal. The F-responses were normal. SNAPs were absent in the ulnar and sural nerves. There was diffuse denervation and reduced motor unit recruitment in the legs. It was concluded that he had a neuropathy with axonal degeneration, with features of a mononeuritis multiplex despite the apparent symmetrical clinical distribution of finding in the limbs. A CAT scan of the chest revealed multiple pulmonary nodules (Fig. 64-1A); lung biopsy showed granulomatous lymphocytic infiltrates with some hemorrhage (see Fig. 64-1B and C). The cells had irregular nuclei. There were both B and T lymphocytes, but mainly T-cells. They appear malignant but a flow cytometry revealed no clear clonicity. Bone marrow biopsy showed similar findings.
The sural nerve biopsy was reviewed and showed evidence of axonal degeneration with lymphocytic infiltrations in the perineural area, some around vessels (see Fig. 64-1D). In some areas, the endoneurium was also infiltrated. The patient was treated with cyclophosmamide which produced remission. Eight months later, he became progressively worse and had multiple organ involvement with lymphocytic infiltrates. He did not respond to aggressive chemotherapy and died. No autopsy was performed.
DISCUSSION This patient had multinodular infiltration of the lungs that appeared to be caused by T-cell non-Hodgkin’s lymphoma that was not well categorized. He had a polyneuropathy, but some nerves were more affected than others, and the nerve biopsy showed pseudovasculitic infiltrates and also axonal degeneration. In
A Man with a Neuropathy, Weight Loss, and Lung Nodules
A
C
B
D
413
FIGURE 64-1 A, Contrast CAT scan of the chest showing multiple small nodes. B, Lung infiltrates consisting mostly of lymphocytes (H&E stain, ×100). C, Homogenous mononuclear cells in node (H&E stain, ×200). D, Perineural cellular infiltrate in sural nerve (toluidine blue stain, ×200).
some areas, the endoneurium was infiltrated by lymphoid cells. Lymphomas can cause various neurological manifestations, including peripheral neuropathies from a metabolic or infectious process or by paraneoplastic mechanisms and tumor infiltration.1 These include a sensorimotor polyneuropathy, Guillain-Barré syndrome (GBS) and a chronic inflammatory demyelinating polyneuropathy (CIDP), particularly in those with Hodgkin’s lymphoma.1–6 Other manifestations include cranial neuropathies, as in this patient; they could also cause radiculopathies from infiltration of the dura and adjacent nerves. Lymphomas can also cause plexopathies, mononeuropathies, and mononeuritis multiplex.7 Non-Hodgkin’s lymphoma is the most common cause of a lymphomatous neuropathy. Hodgkin’s lymphoma, on the other hand, can also manifest with an autoimmune neuropathy, such as GBS or CIDP. Other manifestations
of a lymphoma include vasculitis, cryoglobulinemia, motor neuron disorders, Isaacs syndrome and stiff-person syndrome.8–11 The term neurolymphomatosis defines a malignant lymphomatous infiltration of nerves causing their focal or diffuse enlargement.12–20 In this the cell types can be defined by flow cytometry and immunohistochemistry. The great majority are B cells; only about 10% represent T cells. Other lymphomatous diseases that affect the nervous system include intravascular B-cell lymphoma or malignant angioendotheliomatosis in which the lymphoma is confined to the lumen of vessels, and this can cause strokes, but sometimes also mononeuropathies.18 Lymphoid granulomatosis is an angiocentric non-neoplastic granulomatous disease associated with Epstein-Barr viral infection that could rarely manifest as a peripheral neuropathy.21,22
414
Case 64
Detailed evaluation on patients with proper diagnostic techniques, particularly bone marrow and lymph node biopsy, are useful in determining, if possible, the exact type of lymphoma for treatment.1
SUMMARY This patient had multiple lung nodules and a neuropathy. On EMG some nerves were more affected than others with axonal degeneration. He had a lymphomatous infiltration of the lungs and peripheral nerves. He initially responded to chemotherapy, but later he developed multiorgan involvement.
IMPORTANT POINTS • The differential diagnosis of patients with lung nodes and peripheral neuropathy includes sarcoidosis, infections, Wegener’s granulomatosis, lymphoid granulomatosis, and tumors, such as lymphoma. • Neurolymphomatosis refers to invasion of peripheral nerves and/or central nervous system lymphoma. • Lymphoma can manifest with polyneuropathy, mononeuropathies, plexopathies or radiculopathy, and, rarely, Guillain-Barré syndrome, chronic inflammatory demyelinating polyradiculoneuropathy and other autoimmune disorders (such as cryoglobulinemia), vasculitis, stiffperson syndrome, and Isaacs syndrome.
REFERENCES
6.
7.
8.
9.
10.
11.
12. 13.
14.
15.
16. 17. 18.
1. Kelly JJ, Karcher DS: Lymphoma and peripheral neuropathy: A clinical review. Muscle Nerve 31:301–313, 2005. 2. Baehring JM, Damek D, Martin EC, et al: Neurolymphomatosis. Neuronocol 5:104–115, 2003. 3. Croft PB, Urich H, Wilkinson M: Peripheral neuropathy of sensorimotor type associated with malignant disease. Brain 90:31–66, 1967. 4. Hunt WE, Bouroncle BA, Meagher JN: Neurological complications of leukemia and lymphomas. J Neurosurg 16:135– 151, 1959. 5. Germignani F, Melli G, Inglese C, Marbini A: Cryoglobulinemia is a frequent cause of peripheral neuropathy in undi-
19. 20. 21.
22.
agnosed referral patients. J Peripher Nerv Syst 7:59–64, 2002. Creange A, Theodorou I, Sabourin JC, et al: Inflammatory neuromuscular disorders associated with chronic lymphoid leukemia: Evidence for clonal B cells within muscle and nerve. J Neurol Sci 137:35–41, 1996. Rahmani M, Birouk N, Amarti A, et al: T-cell lymphoma revealed by a mononeuritis multiplex: Case report and review of literature. Rev Neurol (Paris) 163(4):462–490, 2007. Wada M, Kurita K, Tajima K, et al: A case of inflammatory demyelinating polyradiculoneuropathy associated with T-cell lymphoma. Acta Neurol Scand 107:62–66, 2003. Walk D, Handelsman A, Beckmann E, et al: Mononeuropathy multiplex due to infiltration of lymphoma in hematologic remission. Muscle Nerve 21:823–826, 1998. Ince PG, Shaw PJ, Fawcett PR, Bates D: Demyelinating neuropathy due to primary IgM kappa B cell lymphoma of peripheral nerve. Neurology 37:1231–1235, 1987. Lahrmann H, Albrecht G, Drlicek M, et al: Acquired neuromyotonia and peripheral neuropathy in a patient with Hodgkin’s disease. Muscle Nerve 24:834–838, 2001. Borit A, Altrocchi PH: Recurrent polyneuropathy and neurolymphomatosis. Arch Neurol 24:40–49, 1971. Diamond AL, Thomas FP: Neurolymphomatosis. Medlink: Clinical summaries. 2003. Available at www.medlink.com (retrieved April 14, 2004). Trelles JO, Urquiaga C, Palomino L, Trelles L: Human peripheral neurolymphomatosis (reticuloendothelial polyradiculoneuritis). J Neurol Sci 28:187–202, 1976. Diaz-Arrastia R, Younger DS, Hair L, et al: Neurolymphomatosis: A clinicopathologic syndrome re-emerges. Neurology 42:1136–1141, 1992. Gordon PH, Younger DS: Neurolymphomatosis. Neurology 46:1191–1192, 1996. Grisold W, Drlicek M, Jellinger K: Neurolymphomatosis. Neurology 43:1628–1629, 1992. Vital C, Heraud A, Vital A, et al: Acute mononeuropathy with angiotropic lymphoma. Acta Neuropathol (Berl) 78:105–107, 1989. Borit A, Altrocchi PH: Recurrent polyneuropathy and neurolymphomatosis. Arch Neurol 24:40–49, 1971. Baehring JM, Damek D, Martin EC, et al: Neurolymphomatosis. Neuro-Oncol 5:104–115, 2003. Bone RC, Vernon M, Sobonya RE, Rendon H: Lymphomatoid granulomatosis: Report of a case and review of the literature. Am J Med 65:709–716, 1978. Hogan PJ, Greenberg MK, McCarty GE: Neurologic complications of lymphomatoid granulomatosis. Neurology 31:619–620, 1981.