N: Nervous system

ATC group N for modelers: the endpoint sets the structure, placebo needs its own submodel, and PET occupancy bridges dose to effect.
Modified

September 22, 2026

The level 2 codes in Table 1 run from anesthetics to other nervous system drugs, and the endpoint, not the drug, sets the model structure: processed EEG in N01 [1], daily seizure counts in N03 [2] and bounded PANSS scores in N05 [3] each demand a different likelihood.

On 29 March 1948 John Cade gave lithium citrate to W.B., in manic excitement for five years; W.B. left hospital months later and returned to his old job [4,5].

Table 1: ATC N level 2 codes
Level 2 code Description In plain terms Example drug
N01 Anesthetics Propofol (N01AX10) / bupivacaine (N01BB01)
N02 Analgesics Paracetamol (N02BE01) / morphine (N02AA01)
N03 Antiepileptics Levetiracetam (N03AX14) / lamotrigine (N03AX09)
N04 Anti-Parkinson drugs Levodopa and decarboxylase inhibitor (N04BA02) / pramipexole (N04BC05)
N05 Psycholeptics calming: antipsychotics, anxiolytics, hypnotics Olanzapine (N05AH03) / lorazepam (N05BA06)
N06 Psychoanaleptics stimulating: antidepressants, stimulants, anti-dementia drugs Sertraline (N06AB06) / escitalopram (N06AB10)
N07 Other nervous system drugs Buprenorphine (N07BC01) / varenicline (N07BA03)

Modeling notes

Endpoint. Analysing composite PANSS totals as continuous data discards information and violates the scale’s numerical nature; item response theory models the items instead [3]. Depression trials have been modeled on the HAMD-17 total [6].

Placebo first (N05, N06). Placebo arms in schizophrenia and depression improve over weeks, so a placebo time course is fitted before estimating any drug effect [7].

Easy to overlook. PET occupancy bridges dose and effect in N05: patients with acute extrapyramidal syndromes had higher D2 occupancy than those without [8], and model-based analysis quantifies it against efficacy and those symptoms [9].

Mechanistic extrapolation. Human CNS distribution data are scarce, so physiologically based models combined with microdialysis predict unbound extracellular concentrations at the target site [10]. A separately developed pediatric brain PBPK model predicted CSF concentrations and was checked against CSF observed in children, meningitis included [11].

References

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Björnsson MA, Norberg Å, Kalman S, Karlsson MO, Simonsson USH. A two-compartment effect site model describes the bispectral index after different rates of propofol infusion. Journal of Pharmacokinetics and Pharmacodynamics 2010;37:243–55. https://doi.org/10.1007/s10928-010-9157-1.
[2]
Trocóniz IF, Plan EL, Miller R, Karlsson MO. Modelling overdispersion and Markovian features in count data. Journal of Pharmacokinetics and Pharmacodynamics 2009;36:461–77. https://doi.org/10.1007/s10928-009-9131-y.
[3]
Krekels EHJ, Novakovic AM, Vermeulen AM, Friberg LE, Karlsson MO. Item response theory to quantify longitudinal placebo and paliperidone effects on PANSS scores in schizophrenia. CPT: Pharmacometrics & Systems Pharmacology 2017;6:543–51. https://doi.org/10.1002/psp4.12207.
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Cade JFJ. Lithium salts in the treatment of psychotic excitement. The Medical Journal of Australia 1949;2:349–52. https://doi.org/10.5694/j.1326-5377.1949.tb36912.x.
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López-Muñoz F, Shen WW, D’Ocon P, Romero A, Álamo C. A history of the pharmacological treatment of bipolar disorder. International Journal of Molecular Sciences 2018;19:2143. https://doi.org/10.3390/ijms19072143.
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Gomeni R, Merlo-Pich E. Bayesian modelling and ROC analysis to predict placebo responders using clinical score measured in the initial weeks of treatment in depression trials. British Journal of Clinical Pharmacology 2007;63:595–613. https://doi.org/10.1111/j.1365-2125.2006.02815.x.
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Pilla Reddy V, Kozielska M, Johnson M, Vermeulen A, De Greef R, Liu J, et al. Structural Models Describing Placebo Treatment Effects in Schizophrenia and Other Neuropsychiatric Disorders. Clinical Pharmacokinetics 2011;50:429–50. https://doi.org/10.2165/11590590-000000000-00000.
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Farde L, Nordström A-L, Wiesel F-A, Pauli S, Halldin C, Sedvall G. Positron emission tomographic analysis of central D1 and D2 dopamine receptor occupancy in patients treated with classical neuroleptics and clozapine: Relation to extrapyramidal side effects. Archives of General Psychiatry 1992;49:538–44. https://doi.org/10.1001/archpsyc.1992.01820070032005.
[9]
de Greef R, Maloney A, Olsson-Gisleskog P, Schoemaker J, Panagides J. Dopamine D2 occupancy as a biomarker for antipsychotics: Quantifying the relationship with efficacy and extrapyramidal symptoms. The AAPS Journal 2011;13:121–30. https://doi.org/10.1208/s12248-010-9247-4.
[10]
Yamamoto Y, Danhof M, de Lange ECM. Microdialysis: The key to physiologically based model prediction of human CNS target site concentrations. The AAPS Journal 2017;19:891–909. https://doi.org/10.1208/s12248-017-0050-3.
[11]
Verscheijden LFM, Koenderink JB, de Wildt SN, Russel FGM. Development of a physiologically-based pharmacokinetic pediatric brain model for prediction of cerebrospinal fluid drug concentrations and the influence of meningitis. PLOS Computational Biology 2019;15:e1007117. https://doi.org/10.1371/journal.pcbi.1007117.