Glue-Sniffing Neuropathy: A Case Report

Article information

J Electrodiagn Neuromuscul Dis. 2024;26(1):5-8
Publication date (electronic) : 2024 April 22
doi :
Department of Neurology, Ewha Womans University Mokdong Hospital, Ewha Womans University College of Medicine, Seoul, Korea
Corresponding author: Kee Duk Park Department of Neurology, Ewha Womans University Mokdong Hospital, Ewha Womans University College of Medicine, 1071 Anyangcheon-ro, Yangcheon-gu, Seoul 07985, Korea Tel: +82-2-2650-5298 Fax: +82-2-2650-5958 E-mail:
Received 2023 October 19; Revised 2023 December 17; Accepted 2023 December 19.


Glue, a volatile substance that is illegal as a recreational drug, has been popularly used for decades, and it can serve as a stepping stone for harder drugs. Chronic exposure can lead to substantial damage to several organs, including central and peripheral nervous systems. Glue-sniffing neuropathy has been reported since the 1960s, but with a lower frequency in recent years. We report a 45-year-old man who sniffed glue and presented with symmetrical distal motor weakness and paresthesia. Based on the patient’s inhalation history and initial electrodiagnostic study, we considered toxic neuropathy and demyelinating polyneuropathy in the differential diagnosis. He became chair-bound with repeating glue sniffing, and a following nerve conduction study showed the progression of motor-dominant polyneuropathies with markedly reduced amplitudes. An incomplete response to steroid therapy and recovery with inhalant cessation confirmed the diagnosis of glue-sniffing neuropathy. We conclude that glue, a neurotoxic volatile inhalant, produced glue-sniffing neuropathy with characteristic clinical and electrodiagnostic features.


Illegal drug abuse has emerged as a key social issue, prompting the Korean Ministry of Justice to declare a “war on drugs” in an effort to eradicate the use, distribution, and trade of illegal substances [1]. Historically, even when drug-related crime was less prevalent in Korea, adolescents and young adults found glue to be an easily accessible inhalant [2,3]. The rise in glue inhalation has become a concerning social issue, potentially acting as a gateway to “harder” drugs. Until recently, relatively few Koreans have engaged in the long-term use of volatile inhalants, which can result in mild to severe organ system dysfunction [4]. We present the case of a patient who experienced extensive medical and social problems associated with glue inhalation, focusing primarily on polyneuropathic symptoms.

Case Report

A 45-year-old man with a history of hypertension presented with gait disturbance and bilateral lower limb motor weakness that had persisted for 2 months. He had been abusing inhalants, specifically glue, since his 20s and had been jailed multiple times. The patient had developed severe stress after being robbed, which led to a weight loss of 8 kg over 2 months. While taking prescribed antipsychotic medications, including chlordiazepoxide, lorazepam, and zolpidem, he also consumed alcohol and inhaled glue on a daily basis.

The patient had been unable to squat or stand without assistance for 2 months when he visited our department. On a manual muscle test conducted using the Medical Research Council scale, motor weakness was observed in the distal muscles of the bilateral lower extremities, including hip flexion (grade IV), knee flexion/extension (grade IV/IV), ankle dorsiflexion (grade II), ankle plantarflexion (grade III), and toe dorsiflexion (grade II). The bilateral upper extremities were less affected than the lower limbs. Muscle strength in the bilateral proximal upper limbs was intact, while finger flexion and extension displayed a grade of IV+. Light touch sensation, proprioception, and pain and temperature sensation were grossly intact. Deep tendon reflexes were absent in the bilateral knees and ankles.

Serologic test results revealed no definite abnormalities. The values were as follows: creatine kinase, 143 IU/L (normal range, 0 to 185); vitamin B1, 98.22 ng/mL (normal range, 66.5 to 200); vitamin B12, 594.8 pg/mL (normal range, 232 to 1,245); folic acid, 4.1 ng/mL (normal range, 4.6 to 18.7); and homocysteine, 11.3 μmol/L (normal range, 5.0 to 15.0).

Motor nerve conduction studies (NCS) revealed delayed onset latencies and mildly slowed motor velocities, along with conduction blocks in the bilateral median and ulnar nerves (Table 1). Sensory NCS indicated a slight sensory deficit, characterized by low amplitudes in the right median and bilateral ulnar nerves (Table 1). Needle electromyography demonstrated mild-to-moderate denervation potentials and reduced interference patterns in the right first dorsal interosseous, tibialis anterior, and vastus lateralis muscles. These electrodiagnostic findings are indicative of diffuse motor-dominant sensorimotor neuropathy with some demyelinating characteristics.

Findings of the Initial Nerve Conduction Study

Intravenous pulses of 1 g methylprednisolone were administered over 5 days, resulting in a slight improvement of the bilateral lower limb weakness. Specifically, hip flexion improved to grade IV+, and ankle dorsiflexion increased to grade II/III. Upon discharge, the patient was prescribed a tapered dose of prednisolone, starting at 30 mg. However, he was unable to cease glue inhalation.

One month after his initial discharge, the patient’s motor weakness had regressed to pre-treatment levels, and he reported aggravated symmetric distal paresthesia. During his second hospitalization, a follow-up electrodiagnostic study was conducted, revealing the progression of diffuse, motor-dominant sensorimotor neuropathy. Compared to the initial study, motor NCS showed greater delays in onset latencies and reduced amplitudes in the bilateral upper and lower extremities (Table 2). Sensory NCS of the distal upper and lower extremities could not be obtained (Table 2). The patient underwent a second round of intravenous methylprednisolone pulse therapy. For further management, he consented to be admitted to a hospital specializing in substance use disorders.

Findings of the Follow-up Nerve Conduction Study

Despite attempts to discontinue inhalant use, the patient experienced a recurrently relapsing course in the outpatient setting, accompanied by worsening bilateral hand atrophy. Additionally, he was unable to walk unaided and required the use of a wheelchair. After the steroid dose was tapered to a minimal amount, specifically 10 mg of prednisolone, the patient was lost to follow-up in outpatient care.

About 1 year later, we received a letter from the patient, who informed us that he had surrendered to the police. During his incarceration, without access to the inhalant, he regained the ability to write and walk independently, as his distal muscle weakness improved.

The study received approval from the Institute Review Board of Ewha Womans University Mokdong Hospital (IRB no: 2023-08-024), and the requirement for written informed consent from the patient was waived due to the retrospective nature of the report.


Glue sniffing can be broadly defined as the deliberate inhalation of volatile substances for the purpose of achieving a state of recreational intoxication. A commonly abused volatile substance, glue contains toluene and n-hexane [5]. It is readily available and relatively inexpensive, making it attractive to adolescents and young adults. The initial effects of glue inhalation include euphoria, excitation, dizziness, and mild headache, with rapid onset and short duration. With prolonged abuse, individuals may develop nausea, vomiting, dysarthria, gait disturbance, disorientation, and delusion. Chronic abuse can lead to serious health issues such as myopathy, peripheral neuropathy, and encephalopathy, which are characterized by cognitive impairment, ataxia, seizures, and, in severe cases, coma or death [4,6].

Glue-sniffing neuropathy, also known as n-hexane neuropathy, has been well-established since the 1960s and is characterized by subacute onset and motor-dominant neuropathy [5,7]. However, the differential diagnosis should always include demyelinating polyneuropathies, such as chronic inflammatory demyelinating polyneuropathy (CIDP) [8,9]. In the present case, the initial manifestations were symmetric distal-dominant motor weakness with minimal sensory deficits. Given the clinical manifestations and the progressive, relapsing course, we considered CIDP, while bearing in mind the patient’s history of inhalant use. The patient did not fully respond to steroid therapy, which is commonly used for immunosuppression. Follow-up NCS primarily indicated axonal injury, with less pronounced demyelinating features. Considering his history of inhalant abuse, we clinically diagnosed the patient with toxic polyneuropathy due to glue inhalation. His clinical course was consistent with subacute motor-dominant polyneuropathy, and the electrodiagnostic findings predominantly revealed sensorimotor neuropathies with delayed onset latency or mild conduction block. Moreover, his symptoms improved after he stopped inhaling the substance, which further supported the diagnosis.

The treatment for chronic inhalant abuse, as demonstrated with this patient, involves strict abstinence. No antidote is available for inhalant intoxication; however, counseling, psychiatric intervention, and appropriate social support can be beneficial.

In an era of increasingly prevalent illegal drug abuse in Korea, physicians must be cognizant of the various forms of substance abuse and their clinical manifestations. When evaluating patients with neuropathy, physicians should inquire about the patient’s history of addiction and potentially consider toxic polyneuropathy in the differential diagnosis.


Conflict of Interest

No potential conflict of interest relevant to this article was reported.


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Table 1.

Findings of the Initial Nerve Conduction Study

Nerve site Onset latency (ms) Amplitude (mV) CV (m/sec)
Left Right Left Right Left Right
Motor NCS
  Wrist 4.2* 4.1* 6.8 7.8 - -
  Elbow 9.6 9.3 3.2* 2.6* 41* 43*
  Axilla 12.1 11.8 2.5* 2.3* 52 52
  Wrist 3.1* 3.1* 12.5 11.1 - -
  Below elbow 8.1 9.3 11.7 9.0 46* 37*
  Above elbow 10.0 11.9 7.4* 6.9* 53 46
  Axilla 11.9 13.8 7.3* 6.8* 58 63
  Ankle 6.0 6.6 1.8 2.0 - -
  Below fibula 14.9 16.0 1.0 1.0 37 35
  Ankle 4.1 4.6 10.7 11.6 - -
  Knee 14.4 14.5 3.2 3.5 38 39
Sensory NCS
  Finger-wrist 3.3 3.0 9.2 6.5* 38 37
  Palm-wrist 2.1 1.9 15.7 11.9 32 32
  Wrist-elbow 3.5 3.3 25.4 26.1 54 54
  Elbow-axilla 1.7 1.7 109.7 185.6 57 57
  Finger-wrist 2.1 2.7 2.4* 3.6* 37 23
  Palm-wrist 1.3 1.4 13.7 11.5 37 33
  Wrist-elbow 3.5 2.9 17.2 23.3 54 55
  Elbow-axilla 1.8 2.3 51.8 52.0 56 54
  Calf - - 10.9 13.7 38 37

CV, conduction velocity; NCS, nerve conduction study.

*Abnormal value.

Table 2.

Findings of the Follow-up Nerve Conduction Study

Nerve site Onset latency (ms) Amplitude (mV) CV (m/sec)
Left Right Left Right Left Right
Motor NCS
  Wrist 6.5* 6.2* 0.8* 0.9* - -
  Elbow 11.8 14.1 0.4* 0.4* 42* 29*
  Axilla 14.4 16.4 0.4* 0.4* 50* 52
  Wrist 4.5* 3.7* 3.2* 1.5* - -
  Below elbow 9.9 9.5 2.1* 1.7* 43* 40*
  Above elbow 12.3 13.3 2.3* 1.1* 42* 32*
  Axilla 14.5 16.3 1.9* 1.2* 45* 40*
  Ankle 9.1* 7.8* 1.4* 1.3* - -
  Below fibula 20.6 19.0 0.4 0.2 29* 29*
  Ankle 6.3* 5.7* 3.2* 2.1* - -
  Knee 16.3 16.9 0.6 0.5 36* 34*
Sensory NCS
  Finger-wrist NR* NR* NR* NR* - -
  Wrist-elbow 3.4 3.7 15.4 20.5 49 49
  Elbow-axilla 1.5 1.3 94.6 150.7 62 68
  Finger-wrist NR* NR* NR* NR* - -
  Wrist-elbow 3.2 3.4 11.7* 14.1 48 47
  Elbow-axilla 2.5 1.0 20.6 60.6 42 71
  Calf NR* NR* NR* NR* - -

CV, conduction velocity; NCS, nerve conduction study; NR, no response.

*Abnormal value.